the hormone that the pineal gland secretes is
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A chronobiotic is an agent that can cause phase adjustment of the circadian rhythm (biological body clock). That is, it is a substance capable of therapeutically entraining or re-entraining long-term desynchronized or short-term dissociated circadian rhythms in mammals, or prophylactically preventing their disruption following an environmental insult such as is caused by rapid travel across several time zones. The most widely recognized chronobiotic is the hormone melatonin, secreted at night in both diurnal and nocturnal species. History The concept of chronobiotics arose from the research and characterization of the pineal gland. In 1917, Carey Pratt McCord and Floyd Pierpont Allen at Johns Hopkins University demonstrated that tadpoles hatched in water that contained crushed pineal gland were much lighter in color than tadpoles hatched in normal water. No one could explain this phenomenon, and pineal gland research halted until the 1950s. Mark Altschule and Julian Kitay, both physicians at Harvard, summarized the body of pineal gland literature in the 1950s. Their main conclusion was that pineal gland hormones affected the size of rats' gonads, although the hormones had not yet been identified. Melatonin was originally discovered by Aaron Lerner, a Yale dermatologist, and colleagues, who had hoped it could be used to treat vitiligo. Although melatonin did not prove to be relevant to dermatology treatments, it was quickly confirmed to be secreted by the pineal gland to affect the brain. Further research found that circadian melatonin rhythms persisted under constant darkness, which suggested that light alone is not responsible for the cycle of melatonin secretion. Rather, endogenous melatonin serves to internalize light cues, making melatonin responsible for modulating neuroendocrine functions. The suprachiasmatic nucleus, or SCN, is a small region within the anterior hypothalamus of the brain that is responsible for orienting the organism's internal measurement of time to external time cues like daylight. The SCN was first identified to be the "circadian pacemaker" responsible for generating circadian rhythms in 1972. Both Robert Moore at the University of Chicago and Irving Zucker at the University of California, Berkeley linked the SCN to circadian rhythmicity at the same time by lesioning regions of the brain and observing their effects on circadian rhythms. When the SCN region was lesioned in rodents, the rodents did not exhibit circadian rhythms, which established the SCN as the circadian pacemaker. Robert Moore and David Klein first studied the SCN in the context of melatonin secretion by the pineal gland in 1974. Melatonin has been established as a reliable output of the SCN's timekeeping property, and melatonin research has been coupled with SCN research since 1974. Because melatonin is secreted according to signals to the pineal gland from the SCN, exogenous melatonin taken as a chronobiotic can affect feedback to the SCN and its subsequent circadian rhythms. Types Quiadon Quiadon (mepiprazole dihydrochloride) was one of the first chronobiotics used to affect circadian rhythms in humans. A 3-alkyl pyrazolyl piperazine, Quiadon is a serotonin-depleting tranquilizer. However, the original study performed by H.W. Simpson and colleagues in 1973 delivered inconclusive results,
Chronobiotic
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The epithalamus (: epithalami) is a posterior (dorsal) segment of the diencephalon. The epithalamus includes the habenular nuclei, the stria medullaris, the anterior and posterior paraventricular nuclei, the posterior commissure, and the pineal gland. Functions The function of the epithalamus is to connect the limbic system to other parts of the brain. The epithalamus also serves as a connecting point for the dorsal diencephalic conduction system, which is responsible for carrying information from the limbic forebrain to limbic midbrain structures. Some functions of its components include the secretion of melatonin from the pineal gland (circadian rhythms), regulation of motor pathways and emotions, and how energy is conserved in the body. A study has shown that the lateral habenula, in the epithalamus, produces spontaneous theta oscillatory activity that was correlated with theta oscillation in the hippocampus. The same study also found that the increase in theta waves in both lateral habenula and hippocampus was correlated with increased memory performance in rats. This suggests that the lateral habenula has an interaction with the hippocampus that is involved in hippocampus-dependent spatial information processing. Components The epithalamus is a tiny structure that comprises the habenular trigone, the pineal gland, and the habenular commissure. It is wired with the limbic system and basal ganglia. Species that possess a photoreceptive parapineal organ show asymmetry in the epithalamus at the habenula, to the left (dorsal). Clinical significance Dysfunction of the epithalamus can be related to mood disorders such as major depression, schizophrenia, and sleeping disorders. Low levels of melatonin will typically give rise to mood disorders. Calcification of the epithalamus can be linked to periventricular lesions near the limbic system, and lesions of cortico-subcortical pathways that are involved with schizophrenia. Sleep disorders The epithalamus is associated with sleep disorders like insomnia revolving around circadian rhythms of sleep wake cycles. The close connection of the epithalamus with the limbic system regulates the secretion of melatonin by the pineal gland and the regulation of motor pathways and emotions. The secretion of melatonin happens in a cycle. Secretion is high at night or in the absence of light and low during the day. The suprachiasmatic nucleus in the hypothalamus is responsible for this cycle of secretion from the epithalamus, specifically from the pineal gland. The Circadian timekeeping is driven in cells by the cyclical activity of core clock genes and proteins such as per2/PER2. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. References External links https://web.archive.org/web/20080504165606/ http://isc.temple.edu/neuroanatomy/lab/atlas/pdhn/ NIF Search - Epithalamus via the Neuroscience Information Framework See also Limbic system
Epithalamus
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A pinealoma is a tumor of the pineal gland, a part of the brain that produces melatonin. If a pinealoma destroys the cells of the pineal gland in a child, it can cause precocious puberty. Signs and symptoms The pineal gland produces the hormone melatonin which plays a role in regulating circadian rhythms. A pinealoma may disrupt production of this hormone, and insomnia may result. Frequently, paralysis of upward gaze along with several ocular findings such as convergence retraction nystagmus and eyelid retraction also known as Collier's sign and Light Near Dissociation (pupil accommodates but doesn't react to light) are known collectively as Parinaud's syndrome or Dorsal Mid-brain syndrome, are the only physical symptoms seen. This is caused by the compression of the vertical gaze center in the midbrain tectum at the level of the superior colliculus and cranial nerve III. Work-up usually includes Neuro-imaging as seen on the right. A pinealoma may cause interruption of hypothalamic inhibiting pathways, sometimes leading to beta-hCG secretion and consequent Leydig's cell stimulation (endocrine syndrome). Other symptoms may include hydrocephalus, gait disturbances, and precocious puberty. Cause Pinealomas can be due to proliferation of primary pineocytes (pineocytomas, pineoblastomas), astrocytes (astrocytoma), or germ cells (germinoma). Germinomas are the most common tumor in the pineal gland. Diagnosis Treatment Some pinealomas are treated by radiotherapy, since surgical removal may be impossible due to the location. Radiotherapy can be successful in killing the tumour, and 50% of patients undergoing it survive to old age. Prognosis Of the different types of pinealomas, the type with the most favorable prognosis is the pineocytoma. References External links Endocrine neoplasia Brain tumor
Pinealoma
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Pinealocytes are the main cells contained in the pineal gland, located behind the third ventricle and between the two hemispheres of the brain. The primary function of the pinealocytes is the secretion of the hormone melatonin, important in the regulation of circadian rhythms. In humans, the suprachiasmatic nucleus of the hypothalamus communicates the message of darkness to the pinealocytes, and as a result, controls the day and night cycle. It has been suggested that pinealocytes are derived from photoreceptor cells. Research has also shown the decline in the number of pinealocytes by way of apoptosis as the age of the organism increases. There are two different types of pinealocytes, type I and type II, which have been classified based on certain properties including shape, presence or absence of infolding of the nuclear envelope, and composition of the cytoplasm. Types of pinealocytes Type 1 pinealocytes Type 1 pinealocytes are also known as light pinealocytes because they stain at a low density when viewed under a light microscope and appear lighter to the human eye. These Type 1 cells have been identified through research to have a round or oval shape and a diameter ranging from 7–11 micrometers. Type 1 pinealocytes are typically more numerous in both children and adults than Type 2 pinealocytes. They are also considered to be the more active cell because of the presence of certain cellular contents, including a high concentration of mitochondria. Another finding consistent with Type 1 pinealocytes is the increase in the amount of lysosomes and dense granules present in the cells as the age of the organism increases, possibly indicating the importance of autophagocytosis in these cells. Research has also shown that Type 1 pinealocytes contain the neurotransmitter serotonin, which later is converted to melatonin, the main hormone secreted by the pineal gland. Type 2 pinealocytes Type 2 pinealocytes are also known as dark pinealocytes because they stain at a high density when viewed under a light microscope and appear darker to the human eye. As indicated by research and microscopy, they are round, oval, or elongated cells with a diameter of about 7–11.2 micrometers. The nucleus of a Type 2 pinealocyte contains many infoldings which contain large amounts of rough endoplasmic reticulum and ribosomes. An abundance of cilia and centrioles has also been found in these Type 2 cells of the pineal gland. Unique to the Type 2 is the presence of vacuoles containing 2 layers of membrane. As Type 1 cells contain serotonin, Type 2 cells contain melatonin and are thought to have similar characteristics as endocrine and neuronal cells. Synaptic ribbons Synaptic ribbons are organelles seen in pinealocytes using electron microscopy. Synaptic ribbons are found in pinealocytes in both children and adults, but are not found in human fetuses. Research on rats has revealed more information about these organelles. The characteristic protein of synaptic ribbons is RIBEYE, as revealed by light and electron microscopy. In lower vertebrates, synaptic ribbons serve as a photoreceptive organ, but in upper vertebrates, they serve
Pinealocyte
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Seasonal breeders are animal species that successfully mate only during certain times of the year. These times of year allow for the optimization of survival of young due to factors such as ambient temperature, food and water availability, and changes in the predation behaviors of other species. Related sexual interest and behaviors are expressed and accepted only during this period. Female seasonal breeders will have one or more estrus cycles only when she is "in season" or fertile and receptive to mating. At other times of the year, they will be anestrus, or have a dearth of their sexual cycle. Unlike reproductive cyclicity, seasonality is described in both males and females. Male seasonal breeders may exhibit changes in testosterone levels, testes weight, and fertility depending on the time of year. Seasonal breeders are distinct from opportunistic breeders, that mate whenever the conditions of their environment become favorable, and continuous breeders that mate year-round. Timing of seasonal breeding The breeding season is when seasonal breeders reproduce. Various variables can affect when it occurs. A primary influence on the timing of reproduction is food availability. Organisms generally time especially stressing events of reproduction to occur in sync with increases in food availability. This is not always true, however, both because of the importance of other factors and the invalidation of this generalization. For example, in species reproducing at high latitudes, food availability before breeding is more important than availability during reproduction itself. Other factors can also be responsible. For example, species that are preyed upon frequently may time reproduction to occur out of sync with the peak in density of predators. Physiology The hypothalamus is considered to be the central control for reproduction due to its role in hormone regulation. Hence, factors that determine when a seasonal breeder will be ready for mating affect this tissue. This is achieved specifically through changes in the production of the hormone GnRH. GnRH in turn transits to the pituitary where it promotes the secretion of the gonadotropins LH and FSH, both pituitary hormones critical for reproductive function and behavior, into the bloodstream. Changes in gonadotropin secretion initiate the end of anestrus in females. Day length Seasonal breeding readiness is strongly regulated by length of day (photoperiod) and thus season. Photoperiod likely affects the seasonal breeder through changes in melatonin secretion by the pineal gland that ultimately alter GnRH release by the hypothalamus. Hence, seasonal breeders can be divided into groups based on fertility period. "Long day" breeders cycle when days get longer (spring) and are in anestrus in fall and winter. Some animals that are long day breeders include ring-tailed lemurs, horses, hamsters, groundhogs, and mink. "Short day" breeders cycle when the length of daylight shortens (fall) and are in anestrus in spring and summer. The decreased light during the fall decreases the firing of the retinal nerves, in turn decreasing the excitation of the superior cervical ganglion, which then decreases the inhibition of the pineal gland, finally resulting in an increase in melatonin. This
Seasonal breeder
84936
The blood–brain barrier (BBB) is a highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and the central nervous system, thus protecting the brain from harmful or unwanted substances in the blood. The blood–brain barrier is formed by endothelial cells of the capillary wall, astrocyte end-feet ensheathing the capillary, and pericytes embedded in the capillary basement membrane. This system allows the passage of some small molecules by passive diffusion, as well as the selective and active transport of various nutrients, ions, organic anions, and macromolecules such as glucose and amino acids that are crucial to neural function. The blood–brain barrier restricts the passage of pathogens, the diffusion of solutes in the blood, and large or hydrophilic molecules into the cerebrospinal fluid, while allowing the diffusion of hydrophobic molecules (O2, CO2, hormones) and small non-polar molecules. Cells of the barrier actively transport metabolic products such as glucose across the barrier using specific transport proteins. The barrier also restricts the passage of peripheral immune factors, like signaling molecules, antibodies, and immune cells, into the CNS, thus insulating the brain from damage due to peripheral immune events. Specialized brain structures participating in sensory and secretory integration within brain neural circuits—the circumventricular organs and choroid plexus—have in contrast highly permeable capillaries. Structure The BBB results from the selectivity of the tight junctions between the endothelial cells of brain capillaries, restricting the passage of solutes. At the interface between blood and the brain, endothelial cells are adjoined continuously by these tight junctions, which are composed of smaller subunits of transmembrane proteins, such as occludin, claudins (such as Claudin-5), junctional adhesion molecule (such as JAM-A). Each of these tight junction proteins is stabilized to the endothelial cell membrane by another protein complex that includes scaffolding proteins such as tight junction protein 1 (ZO1) and associated proteins. The BBB is composed of endothelial cells restricting passage of substances from the blood more selectively than endothelial cells of capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as "glia limitans") surround the endothelial cells of the BBB, providing biochemical support to those cells. The BBB is distinct from the quite similar blood-cerebrospinal fluid barrier, which is a function of the choroidal cells of the choroid plexus, and from the blood-retinal barrier, which can be considered a part of the whole realm of such barriers. Not all vessels in the human brain exhibit BBB properties. Some examples of this include the circumventricular organs, the roof of the third and fourth ventricles, capillaries in the pineal gland on the roof of the diencephalon and the pineal gland. The pineal gland secretes the hormone melatonin "directly into the systemic circulation", thus melatonin is not affected by the blood–brain barrier. Development The BBB appears to be functional by the time of birth. P-glycoprotein, a transporter, exists already in the embryonal endothelium. Measurement of brain uptake of various blood-borne solutes showed that newborn endothelial cells were functionally similar to
Blood–brain barrier
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The history of the pineal gland is an account of the scientific development on the understanding of the pineal gland from the ancient Greeks that led to the discovery of its neuroendocrine properties in the 20th century CE. As an elusive and unique part of the brain, the pineal gland has the longest history among the body organs as a structure of unknown function – it took almost two millennia to discover its biological roles. Until the 20th century, it was recognised with a mixture of mysticism and scientific conjectures as to its possible nature. The ancient Greeks visualised the pineal gland as a sort of guard (valve), like the pylorus of stomach, that regulate the flow of pneuma (vital spirits) in the brain. Galen of Pergamum in the 2nd century CE was the first to make written record of the gland and argued against the prevailing concept. According to him, the gland has no spiritual or physiological role, but merely a supporting organ of the brain, and gave the name κωνάριο (konario, often Latinised as conarium) for its cone-shaped appearance. Galen's description remained a scientific concept until the Renaissance when alternative explanations were postulated. By then, the Latin name glandula pinealis became a common usage. René Descartes's description as the "seat of the soul" in the 17th century became one of the most influential concepts for the next three centuries. The biological role of the pineal gland was first discovered in 1958 when dermatologist Aaron B. Lerner and colleagues discovered a skin-lightening factor, which they named melatonin. Lerner's team found the chemical compound from the cow pineal extract that could lightens the skin of frog. It was subsequently discovered that melatonin is a hormone that regulates day-night cycle (circadian rhythm), and modulates other organs. The pineal gland thereby was established as an endocrine gland. As it controls other the important endocrine glands, including the so-called "master gland", the pituitary gland, it is more appropriate to refer the pineal gland as the true "master gland" of the body. Ancient Greeks Greek physician Galen was the first to give written description about the pineal gland in the 2nd century CE. He indicated that the structure as an part of the brain was already known to earlier Greek scholars, crediting Herophilus (325–280 BCE) as the first to have described the possible role of the gland. Herophilus had explained that the structure was a kind of valve, like the pylorus of stomach that controls the amount of food particles moving into the intestine. As a valve in the brain, the structure guards the brain chambers and maintains the right amount of the flow of vital spirits called pneuma. It was conceived as a guardian or housekeeper that regulates the movement of vital spirits from the middle (now identified to be the third) ventricle to the one in the parencephalis (fourth ventricle). The idea was generally endorsed by other Greek scholars. Galen made the description of the pineal gland in his two books De
History of the pineal gland
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Melatonin receptors are G protein-coupled receptors (GPCR) which bind melatonin. Three types of melatonin receptors have been cloned. The MT1 (or Mel1A or MTNR1A) and MT2 (or Mel1B or MTNR1B) receptor subtypes are present in humans and other mammals, while an additional melatonin receptor subtype MT3 (or Mel1C or MTNR1C) has been identified in amphibia and birds. The receptors are crucial in the signal cascade of melatonin. In the field of chronobiology, melatonin has been found to be a key player in the synchrony of biological clocks. Melatonin secretion by the pineal gland has circadian rhythmicity regulated by the suprachiasmatic nucleus (SCN) found in the brain. The SCN functions as the timing regulator for melatonin; melatonin then follows a feedback loop to decrease SCN neuronal firing. The receptors MT1 and MT2 control this process. Melatonin receptors are found throughout the body in places such as the brain, the retina of the eye, the cardiovascular system, the liver and gallbladder, the colon, the skin, the kidneys, and many others. In 2019, X-ray crystal and cryo-EM structures of MT1 and MT2 were reported. History Melatonin has been known about since the beginning of the 20th century with experiments led by Carey P. McCord and Floyd P. Allen. The two scientists obtained extracts of the pineal gland from bovines and noticed its blanching effects on the skin of tadpoles. The melatonin chemical was found and isolated in the pineal gland in 1958 by physician Aaron B. Lerner. Due to its ability to lighten skin, Lerner named the compound melatonin. Discovery of high affinity binding sites for melatonin were found near the end of the 20th century. The experiment to find these binding sites utilized an expression cloning strategy to isolate the site. The receptor was first cloned from the melanophores of Xenopus laevis. In recent years, research with melatonin has shown to improve neurological disorders such as Parkinson's, Alzheimer's disease, brain edema, and traumatic brain injury, alcoholism, and depression. Also, regulation of addictive behavior has been associated with the increase of melatonin receptor-related cAMP in the mesolimbic dopaminergic system. Melatonin treatment has also been studied as a remedy of disturbed circadian rhythms found in conditions such a jet lag, shift work, and types of insomnia. Function and regulation General Melatonin serves a variety of functions throughout the body. While its role in sleep promotion is its most well known, melatonin has its hands in a wide range of biological processes. In addition to sleep promotion, melatonin also regulates hormone secretion, rhythms in reproductive activity, immune functionality, and circadian rhythms. Further, melatonin functions as a neuroprotective, pain-reducer, tumor suppressor, reproduction stimulant, and antioxidant. Melatonin has an anti-excitatory effect on brain activity which is exemplified by its reduction of epileptic activity in children which is to say that it is an inhibitory transmitter. The functional diversity of the melatonin receptors contribute to the range of influence that melatonin has over various biological processes. Some of the functions/effects of melatonin binding to its receptor have been
Melatonin receptor
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Journal of Pineal Research is a peer-reviewed scientific journal covering research on the pineal gland and its hormonal products, chiefly melatonin, in all vertebrate species. Experimental studies on circadian rhythms and sleep are also published by the journal. It is published by John Wiley & Sons and the editor-in-chief is Gianluca Tosini. According to the Journal Citation Reports, the journal has a 2020 impact factor of 13.007. References External links Endocrinology journals Wiley (publisher) academic journals Academic journals established in 1984 English-language journals Physiology journals Neuroscience journals
Journal of Pineal Research
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In the context of human evolution, human vestigiality involves those traits occurring in humans that have lost all or most of their original function through evolution. Although structures called vestigial often appear functionless, a vestigial structure may retain lesser functions or develop minor new ones. In some cases, structures once identified as vestigial simply had an unrecognized function. Vestigial organs are sometimes called rudimentary organs. Many human characteristics are also vestigial in other primates and related animals. History Charles Darwin listed a number of putative human vestigial features, which he termed rudimentary, in The Descent of Man (1871). These included the muscles of the ear; wisdom teeth; the appendix; the tail bone; body hair; and the semilunar fold in the corner of the eye. Darwin also commented on the sporadic nature of many vestigial features, particularly musculature. Making reference to the work of the anatomist William Turner, Darwin highlighted a number of sporadic muscles which he identified as vestigial remnants of the panniculus carnosus, particularly the sternalis muscle. In 1893, Robert Wiedersheim published The Structure of Man, a book on human anatomy and its relevance to man's evolutionary history. This book contained a list of 86 human organs that he considered vestigial, or as Wiedersheim himself explained: "Organs having become wholly or in part functionless, some appearing in the Embryo alone, others present during Life constantly or inconstantly. For the greater part Organs which may be rightly termed Vestigial." His list of supposedly vestigial organs included many of the examples on this page as well as others then mistakenly believed to be purely vestigial, such as the pineal gland, the thymus gland, and the pituitary gland. Some of these organs that had lost their obvious, original functions later turned out to have retained functions that had gone unrecognized before the discovery of hormones or many of the functions and tissues of the immune system. Examples included: the role of the pineal in the regulation of the circadian rhythm (neither the function nor even the existence of melatonin was yet known); discovery of the role of the thymus in the immune system lay many decades in the future; it remained a mystery organ until after the mid-20th century; the pituitary and hypothalamus with their many and varied hormones were far from understood, let alone the complexity of their interrelationships. Historically, there was a trend not only to dismiss the appendix as being uselessly vestigial, but an anatomical hazard, a liability to dangerous inflammation. As late as the mid-20th century, many reputable authorities conceded it no beneficial function. This was a view supported, or perhaps inspired, by Darwin himself in the 1874 edition of his book The Descent of Man, and Selection in Relation to Sex. The organ's patent liability to appendicitis and its poorly understood role left the appendix open to blame for a number of possibly unrelated conditions. For example, in 1916, a surgeon claimed that removal of the appendix had cured several cases of trifacial neuralgia and other nerve
Human vestigiality
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Melatonin receptor type 1A is a protein that in humans is encoded by the MTNR1A gene. Function This gene encodes the MT1 protein, one of two high-affinity forms of a receptor for melatonin, the primary hormone secreted by the pineal gland. This receptor is a G protein-coupled, 7-transmembrane receptor that is responsible for melatonin effects on mammalian circadian rhythm and reproductive alterations affected by day length. The receptor is an integral membrane protein that is readily detectable and localized to two specific regions of the brain. The hypothalamic suprachiasmatic nucleus appears to be involved in circadian rhythm while the hypophysial pars tuberalis may be responsible for the reproductive effects of melatonin. Ligands Melatonin – full agonist Afobazole – agonist Agomelatine – agonist See also Melatonin receptor Discovery and development of melatonin receptor agonists References Further reading G protein-coupled receptors Human proteins 1A
Melatonin receptor 1A
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Pineoblastoma is a malignant tumor of the pineal gland. A pineoblastoma is a supratentorial midline primitive neuroectodermal tumor. Pineoblastoma can present at any age, but is most common in young children. They account for 0.001% of all primary CNS neoplasms. Epidemiology Pineoblastomas typically occur at very young ages. One study found the average age of presentation to be 4.3 years, with peaks at age 3 and 8. Another cites cases to more commonly occur in patients under 2 years of age. Rates of occurrence for males and females are similar, but may be slightly more common in females. One study found incidence of pineoblastoma to be increased in black patients compared to white patients by around 71%. This difference was most apparent in patients aged 5 to 9 years old. Pathophysiology The pineal gland is a small organ in the center of the brain that is responsible for controlling melatonin secretion. Several tumors can occur in the area of the pineal gland, with the most aggressive being pineoblastoma. Pineoblastomas arise from embryonal cells in the pineal gland and are rapidly growing. They are considered grade 4 tumors, meaning they are malignant and may metastasize. Due to the pineal gland's location at the center of the brain and the rapidly growing nature of this disease, obstruction of CNS fluid is a common symptom. The exact cause of pineoblastoma is unknown. MicroRNA dysregulation has been found to be associated with many cases of pineoblastoma, specifically, mutations in DICER1 and DROSHA genes. DICER1 germline mutations cause a tumor predisposition syndrome, and should be considered in patients with pineoblastoma. Pineoblastoma may occur in patients with hereditary uni- or bilateral retinoblastoma. When retinoblastoma patients present with pineoblastoma this is characterized as "trilateral retinoblastoma". Up to 5% of patients with hereditary retinoblastoma are at risk of developing trilateral retinoblastoma. This tumor combination is more aggressive than an isolated pineoblastoma. Prognosis of patients with trilateral retinoblastoma is dismal, only a few patients have survived more than 5 years after diagnosis; all survivors were diagnosed with small tumors in a subclinical stage. Recent advances in (high-dose) chemotherapy treatment regimens and early detection have improved survival of patients with trilateral retinoblastoma to up to 50%. Additionally, various mutations or deletions in chromosomes 1, 9, 13, 16 and 22 have been associated with pineoblastoma incidence. Clinical features The most common symptoms to occur with pineoblastoma are headache, behavior changes, and cognitive disturbances. These masses also often cause obstructive hydrocephalus, leading to increased intracranial pressure. This can result in vision changes and Parinaud's syndrome. Due to the aggressive nature of the disease, tumor spread at the time of diagnosis is common. Pineoblastomas often invades locally, with spread to the head and spine seen in 25–41% of patients. While CNS spread is relatively common, these tumors rarely cause distant metastases. Diagnosis Several imaging methods can be used to diagnose pineoblastoma. Initially, urgent CTs are recommended, followed by MR imaging. CT will show large, multilobulated masses with heterogenous contrast enhancement and peripheral calcification
Pineoblastoma
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Pineocytoma, is a rare, benign, slowly growing tumor of the pineal gland. The pineal gland is a small endocrine gland close to the center of the brain that secretes melatonin into the bloodstream. Pineocytomas can cause pressure and fluid build-up in the brain. They are more common in adults. Symptoms include vision problems, nausea, vomiting, memory problems, and headaches. Signs and symptoms Because of their massive growth, pineocytoma symptoms are related to increased intracranial pressure. Some common symptoms of pineocytomas include Parinaud syndrome, headaches, dizziness, papilledema, tremors, ataxia, impaired vision, ambulation, ptosis, nausea, and vomiting. Causes The true cause of pineocytomas is unknown. No genetic mutations have been linked to pineocytomas however, there have been some associations with certain chromosomal abnormalities. There are no known risk factors for pineocytomas. Diagnosis Pineocytomas typically present on a CT scan as round and well-delineated masses with a diameter under 3cm. Pineocytomas are homogeneous, hypodense, and sometimes have central or peripheral calcification. On an MRI a pineocytoma often appears isointense or hypointense in T1-weighted scans. However, they usually appear hyperintense on T2-weighted scans. The diagnosis of a pineocytoma is confirmed by a brain biopsy. Management The main treatment options for pineocytomas are gross total resection, subtotal resection, and radiation. See also Pineal gland References External links Endocrine neoplasia Brain tumor
Pineocytoma
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Melatonin receptor 1B, also known as MTNR1B, is a protein that in humans is encoded by the MTNR1B gene. Function This gene encodes the MT2 protein, one of two high-affinity forms of a receptor for melatonin, the primary hormone secreted by the pineal gland. This gene product is an integral membrane protein that is a G-protein coupled, 7-transmembrane receptor. It is found primarily in the retina and brain; however, this detection requires RT-PCR. It is thought to participate in light-dependent functions in the retina and may be involved in the neurobiological effects of melatonin. Besides the brain and retina this receptor is expressed on the bone forming cells where it regulates their function in depositing bone. Clinical significance Several studies have identified MTNR1B receptor mutations that are associated with increased average blood sugar level and around a 20 percent elevated risk of developing type 2 diabetes. MTNR1B mRNA is expressed in human islets, and immunocytochemistry confirms that it is primarily localized in beta cells in islets. Ligands The following MT2R ligands have selectivity over MT1R: Compound 3d: antagonist with sub-nM affinity Compound 18f: antagonist and compound 18g partial agonist: sub-nM affinity, >100-fold selectivity over MT1 Compound 14: antagonist Compound 13: agonist See also Melatonin receptor Discovery and development of melatonin receptor agonists References Further reading External links G protein-coupled receptors Human proteins 1B
Melatonin receptor 1B
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Rick Strassman is an American clinical associate professor of psychiatry at the University of New Mexico School of Medicine. He has held a fellowship in clinical psychopharmacology research at the University of California San Diego and was Professor of Psychiatry for eleven years at the University of New Mexico. After 20 years of intermission, Strassman was the first person in the United States to undertake human research with psychedelic, hallucinogenic, or entheogenic substances with his research on N,N-dimethyltryptamine, also known as DMT. He is also the author of DMT: The Spirit Molecule, which summarizes his academic research into DMT and other experimental studies of it, and includes his own reflections and conclusions based on this research. Life and education Strassman was born in Los Angeles, California, on February 8, 1952, to a Conservative Jewish family. He graduated from Ulysses S. Grant High School in Van Nuys in 1969. He studied zoology at Pomona College in Claremont for two years before transferring to Stanford University, where he graduated with departmental honors in biological sciences in 1973. He continued laboratory research at Stanford before attending Albert Einstein College of Medicine of Yeshiva University in New York, where he graduated with an M.D. with departmental honors, specializing in psychiatry. He began his general psychiatry residency at the University of California, Davis, where he received the Sandoz Award for outstanding graduating resident in 1981. From 1982 to 1983, he trained as a fellow in clinical psychopharmacology research at the University of California, San Diego. He then served on the clinical faculty in the psychiatry department at UC Davis Medical Center, before becoming an assistant professor in the psychiatry department at the University of New Mexico School of Medicine in Albuquerque in 1984. At UNM, Strassman researched the function of the pineal gland. His research group documented the first known role of melatonin in humans. He became clinical associate professor of psychiatry in 1991. He has published over 40 peer-reviewed scientific articles on psychopharmacology, neurology, psychiatry, neuroendocrinology and neuropsychopharmacology. Developmental biology research As an undergraduate at Stanford, working in the developmental biology laboratory of Norman K. Wessells, Strassman developed a new model for growing embryonic avian dorsal root ganglion neurons, suspended in a semi-solid agar matrix, thus allowing three-dimensional assessment of growing patterns. Using this model, he discovered a nonrandom pattern of growth of the leading edge of these cells. Melatonin research Strassman's interest in the human biology of altered states of consciousness led him to study the pineal gland hormone melatonin in the 1980s, at which time there were suggestive data regarding its psychoactive effects. This research took place at the University of New Mexico's School of Medicine in Albuquerque, where he became a tenured associate professor of psychiatry. He first developed a model of all-night suppression of melatonin by all-night bright light. He then established a successful exogenous melatonin infusion protocol that replicated endogenous melatonin levels in the bright-light conditions. All-night bright-light suppression of melatonin suppressed the normal trough of body temperature seen
Rick Strassman
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Thomas Alvin Wehr is an American psychiatrist, research scientist, and author. He is a scientist emeritus and former chief of the Clinical Psychobiology branch of the National Institute of Mental Health (NIMH). Education Wehr received his degree in medicine from the University of Louisville School of Medicine in 1969. He subsequently completed his psychiatric residency at Yale School of Medicine and an internship at Michael Reese Hospital. Research In a 1990s study on photoperiodicity in humans, Wehr placed a group of volunteers in an environment in which it was dark for 14 hours each day for a month. The subjects were able to sleep as much as they wanted during the experiment. On the first night, the subjects slept an average of 11 hours a night. This was concluded to be probably repaying a chronic sleep debt. By the fourth week, the subjects slept an average of eight hours a nightbut in two separate blocks. First, subjects tended to lie awake for one to two hours and then fall quickly asleep. The onset of sleep was linked to a spike in the hormone melatonin, whose secretion by the brain's pineal gland is triggered by darkness. After an average of three to five hours of sleep, the subjects would awaken and spend an hour or two in quiet wakefulness before a second three- to five-hour sleep period. It was thus suggested that such a biphasic pattern of sleep is the natural or pre-historic tendency for humans. No research into the sleeping patterns in natural environments of primates closely related to humans was cited for comparison. Wehr and colleague Norman E. Rosenthal are credited with identifying and describing Seasonal Affective Disorder (SAD) and developing light therapy to treat it. Wehr and colleague Anna Wirz-Justice were awarded the Anna Monika Prize for their work in the chronobiology of depressive illness. They carried out the first sleep phase advance experiment in a bipolar patient. Wehr was the co-author of Circadian Rhythms in Psychiatry (Psychobiology and Psychopathology) with Frederick Goodwin, and How to Beat Jet Lag (1993) with D.A. Oren, W. Reich, and N. Rosenthal. See also Segmented sleep References External links "Rethinking Sleep," "The New York Times", September 22, 2012 "Modern Life Suppresses an Ancient Body Rhythm," The New York Times, March 14, 1995 Various Articles, The New York Times Various Interviews, National Public Radio (NPR) "Body Clocks," The Infinite Mind, February 20, 2008 American psychiatrists Sleep researchers National Institutes of Health people Chronobiologists Living people Yale School of Medicine alumni Year of birth missing (living people) University of Louisville School of Medicine alumni
Thomas Wehr
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6-Hydroxymelatonin (6-OHM) is a naturally occurring, endogenous, major active metabolite of melatonin. Similar to melatonin, 6-OHM is a full agonist of the MT1 and MT2 receptors. It is also an antioxidant and neuroprotective, and is even more potent in this regard relative to melatonin. See also N-Acetylserotonin (normelatonin) 5-Methoxytryptamine References Acetamides Antioxidants Biogenic amines Circadian rhythm Hormones of the pineal gland Melatonin receptor agonists Neuroprotective agents Neurotransmitters Phenols Tryptamine alkaloids Mexamines
6-Hydroxymelatonin
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Brain-specific homeobox is a protein that in humans is encoded by the BSX gene. Structure and expression pattern Bsx is an evolutionarily highly-conserved homeodomain-containing transcription factor that belongs to the ANTP-class. In mouse it has been shown to be expressed in the telencephalic septum, pineal gland, the mammillary bodies and arcuate nucleus. Function in the hypothalamus In the hypothalamic arcuate nucleus, Bsx has been demonstrated to be necessary for normal expression levels of the two orexigenic neuropeptides Agouti-related peptide and Neuropeptide Y. Function in the pineal gland In the pineal gland of the clawed frog Xenopus, Bsx is expressed following the circadian rhythm and controls photoreceptor cell differentiation. In zebrafish Bsx is required for normal development of all cell types within the pineal gland, including melatonin-releasing pinealocytes, photoreceptor cells and leftwards migrating parapineal cells, which in zebrafish are crucial for the establishment of brain asymmetry. References Brain Proteins Transcription factors Genes Molecular biology
Brain-specific homeobox
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Pulsatile secretion is a biochemical phenomenon observed in a wide variety of cell and tissue types, in which chemical products are secreted in a regular temporal pattern. The most common cellular products observed to be released in this manner are intercellular signaling molecules such as hormones or neurotransmitters. Examples of hormones that are secreted pulsatilely include insulin, thyrotropin, TRH, gonadotropin-releasing hormone (GnRH) and growth hormone (GH). In the nervous system, pulsatility is observed in oscillatory activity from central pattern generators. In the heart, pacemakers are able to work and secrete in a pulsatile manner. A pulsatile secretion pattern is critical to the function of many hormones in order to maintain the delicate homeostatic balance necessary for essential life processes, such as development and reproduction. Variations of the concentration in a certain frequency can be critical to hormone function, as evidenced by the case of GnRH agonists, which cause functional inhibition of the receptor for GnRH due to profound downregulation in response to constant (tonic) stimulation. Pulsatility may function to sensitize target tissues to the hormone of interest and upregulate receptors, leading to improved responses. This heightened response may have served to improve the animal's fitness in its environment and promote its evolutionary retention. Pulsatile secretion in its various forms is observed in: Hypothalamic-pituitary-gonadal axis (HPG) related hormones Glucocorticoids Insulin Growth hormone Parathyroid hormone Neuroendocrine Pulsatility Nervous system control over hormone release is based in the hypothalamus, from which the neurons that populate the pariventricular and arcuate nuclei originate. These neurons project to the median eminence, where they secrete releasing hormones into the hypophysial portal system connecting the hypothalamus with the pituitary gland. There, they dictate endocrine function via the four Hypothalamic-Pituitary-Glandular axes. Recent studies have begun to offer evidence that many pituitary hormones which have been observed to be released episodically are preceded by pulsatile secretion of their associated releasing hormone from the hypothalamus in a similar pulsatile fashion. Novel research into the cellular mechanisms associated with pituitary hormone pulsatility, such as that observed for Leutinizing Hormone (LH) and Follicle Stimulating Hormone (FSH), have indicated similar pulses into the hypophyseal vessels of Gonadotropin Releasing Hormone (GnRH). Luteinizing Hormone & Follicle Stimulating Hormone (HPG axis) LH is released from the pituitary gland along with FSH in response to GnRH release into the hypophyseal portal system. Pulsatile GnRH release causes pulsatile LH and FSH release to occur, which modulates and maintains appropriate levels of bioavailable gonadal hormone: testosterone in males and estradiol in females subject to the requirements of a superior feedback loop. In females the levels of LH is typically 1–20 IU/L during the reproductive period and is estimated to be 1.8–8.6 IU/L in males over 18 years of age. ACTH and Glucocorticoids (HPA axis) Regular pulses of glucocorticoids, mainly cortisol in the case of humans, are released regularly from the adrenal cortex following a circadian pattern in addition to their release as a part of the stress response. Cortisol release follows a high frequency of pulses forming an ultradian rhythm,
Pulsatile secretion
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Circumventricular organs (CVOs) (circum-: around ; ventricular: of ventricle) are structures in the brain characterized by their extensive and highly permeable capillaries, unlike those in the rest of the brain where there exists a blood–brain barrier (BBB) at the capillary level. Although the term "circumventricular organs" was originally proposed in 1958 by Austrian anatomist Helmut O. Hofer concerning structures around the brain ventricular system, the penetration of blood-borne dyes into small specific CVO regions was discovered in the early 20th century. The permeable CVOs enabling rapid neurohumoral exchange include the subfornical organ (SFO), the area postrema (AP), the vascular organ of lamina terminalis (VOLT — also known as the organum vasculosum of the lamina terminalis (OVLT)), the median eminence, the pituitary neural lobe, and the pineal gland. The circumventricular organs are midline structures around the third and fourth ventricles that are in contact with blood and cerebrospinal fluid, and they facilitate special types of communication between the central nervous system and peripheral blood. Additionally, they are an integral part of neuroendocrine function. Highly permeable capillaries allow the CVOs to act as an alternative route for peptides and hormones in the neural tissue to sample from and secrete to circulating blood. CVOs also have roles in body fluid regulation, cardiovascular functions, immune responses, thirst, feeding behavior and reproductive behavior. CVOs can be classified as either sensory or secretory organs serving homeostatic functions and body water balance. The sensory organs include the area postrema, the subfornical organ, and the vascular organ of lamina terminalis, all having the ability to sense signals in blood, then pass that information neurally to other brain regions. Through their neural circuitry, they provide direct information to the autonomic nervous system from the systemic circulation. The secretory organs include the subcommissural organ (SCO), the pituitary gland, the median eminence, and the pineal gland. These organs are responsible for secreting hormones and glycoproteins into the peripheral blood using feedback from both the brain environment and external stimuli. Circumventricular organs contain capillary networks that vary between one another and within individual organs both in density and permeability, with most CVO capillaries having a permeable endothelial cell layer, except for those in the subcommissural organ. Furthermore, all CVOs contain neural tissue, enabling a neuroendocrine role. Although the choroid plexus also has permeable capillaries, it does not contain neural tissue; rather, its primary role is to produce cerebrospinal fluid (CSF), and therefore is typically not classified as a CVO. Sensory organs Area postrema Anatomy The area postrema is located in the caudal medulla oblongata near the junction of the brainstem and the spinal cord. In humans and in most other mammals that have been studied, it consists of swellings on either wall of the fourth ventricle. In rodents and lagomorphs, however, the area postrema forms a midline structure dorsal to the obex. When viewed histologically for its capillary distribution and morphology, the area postrema has numerous subregions separated according to capillary permeability, rates of blood flow, and duration of blood transit through
Circumventricular organs
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Non-tropic hormones are hormones that directly stimulate target cells to induce effects. This differs from the tropic hormones, which act on another endocrine gland. Non-tropic hormones are those that act directly on targeted tissues or cells, and not on other endocrine gland to stimulate release of other hormones. Many hormones act in a chain reaction. Tropic hormones usually act in the beginning of the reaction stimulating other endocrine gland to eventually release non-tropic hormones. These are the ones that act in the end of the chain reaction on other cells that are not part of other endocrine gland. The Hypothalamic-pituitary-adrenal axis is a perfect example of this chain reaction. The reaction begins in the hypothalamus with a release of corticotropin-releasing hormone/factor (CRH/F; tropic). This stimulates the anterior pituitary and causes it to release Adrenocorticotropic hormone (ACTH; tropic) to the adrenal glands. Lastly, cortisol (non-tropic) is secreted from the adrenal glands and goes into the bloodstream where it can have more widespread effects on organs and tissues. Since cortisol is what finally reaches other tissues in the body, it is a non-tropic hormone. CRH and ACTH are tropic hormones because they act on the anterior pituitary gland and adrenal glands, respectively, both of which are endocrine glands. Non-tropic hormones are thus often the last piece of a larger process and chain of hormone secretion. Both tropic and non-tropic hormones are necessary for proper endocrine function. For example, if ACTH (Adrenocorticotropin hormone; a tropic hormone) is inhibited, cortisol can no longer be released because the chain reaction has been interrupted. Some examples of non-tropic hormones are: Glucocorticoids: secreted from the adrenal glands and released directly into the blood stream where it alters blood glucose levels. Glucocorticoids, including hormones such as cortisol and corticosterone, are highly involved in the stress response, and are often referred to as the stress hormones. In the case of chronic stress, glucocorticoids can be very damaging to memory. Vasopressin (Antidiuretic hormone; ADH): secreted from the posterior pituitary and acts on the kidneys to maintain water balance in the body. Oestrogen: secreted from the ovaries and aid in fetal development as well as development of secondary sexual characteristics in females. Testosterone: secreted from the testes, testosterone influences not only gonadal development, but aggressive behavior, sexual behavior, and masculinization of males. Oxytocin: secreted from the posterior pituitary and acts on the uterus and mammary glands to produce contractions. It is also involved in pair bonding and sexual selection and behaviors. Epinephrine and Norepinephrine: secreted from the adrenal medulla and acts on the heart, liver, and blood vessels primarily in acute stress situations. They are key components of the processes involved in the sympathetic nervous system. Since they are involved in arousal, stress, and often physical exercise some of these hormones are also called stress hormones. Most endocrine glands, such as the gonads, pancreas, and adrenal glands, produce non-tropic hormones. Those released from the pituitary gland in the brain include: See also Endocrine system Tropic hormone References Sources Biology 12 McGraw
Non-tropic hormone
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Parathyroid glands are small endocrine glands in the neck of humans and other tetrapods. Humans usually have four parathyroid glands, located on the back of the thyroid gland in variable locations. The parathyroid gland produces and secretes parathyroid hormone in response to low blood calcium, which plays a key role in regulating the amount of calcium in the blood and within the bones. Parathyroid glands share a similar blood supply, venous drainage, and lymphatic drainage to the thyroid glands. Parathyroid glands are derived from the epithelial lining of the third and fourth pharyngeal pouches, with the superior glands arising from the fourth pouch and the inferior glands arising from the higher third pouch. The relative position of the inferior and superior glands, which are named according to their final location, changes because of the migration of embryological tissues. Hyperparathyroidism and hypoparathyroidism, characterized by alterations in the blood calcium levels and bone metabolism, are states of either surplus or deficient parathyroid function. Structure The parathyroid glands are two pairs of glands usually positioned behind the left and right lobes of the thyroid. Each gland is a yellowish-brown flat ovoid that resembles a lentil seed, usually about 6 mm long and 3 to 4 mm wide, and 1 to 2 mm anteroposteriorly. There are typically four parathyroid glands. The two parathyroid glands on each side which are positioned higher are called the superior parathyroid glands, while the lower two are called the inferior parathyroid glands. Healthy parathyroid glands generally weigh about 30 mg in men and 35 mg in women. These glands are not visible or able to be felt during examination of the neck. Each parathyroid vein drains into the superior, middle and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior thyroid vein drains into the brachiocephalic vein. Lymphatic drainage Lymphatic vessels from the parathyroid glands drain into deep cervical lymph nodes and paratracheal lymph nodes. Variation The parathyroid glands are variable in number: three or more small glands, and can usually be located on the posterior surface of the thyroid gland. Occasionally, some individuals may have six, eight, or even more parathyroid glands. Rarely, the parathyroid glands may be within the thyroid gland itself, the chest, or even the thymus. Microanatomy The parathyroid glands are named for their proximity to the thyroid—and serve a completely different role than the thyroid gland. The parathyroid glands are quite easily recognizable from the thyroid as they have densely packed cells, in contrast with the follicular structure of the thyroid. Two unique types of cells are present in the parathyroid gland: Chief cells, which synthesize and release parathyroid hormone. These cells are small, and appear dark when loaded with parathyroid hormone, and clear when the hormone has been secreted, or in their resting state. Oxyphil cells, which are lighter in appearance and increase in number with age, have an unknown function. Development In the early development of the human embryo, a series of five
Parathyroid gland
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A biological system is a complex network which connects several biologically relevant entities. Biological organization spans several scales and are determined based different structures depending on what the system is. Examples of biological systems at the macro scale are populations of organisms. On the organ and tissue scale in mammals and other animals, examples include the circulatory system, the respiratory system, and the nervous system. On the micro to the nanoscopic scale, examples of biological systems are cells, organelles, macromolecular complexes and regulatory pathways. A biological system is not to be confused with a living system, such as a living organism. Organ and tissue systems These specific systems are widely studied in human anatomy and are also present in many other animals. Respiratory system: the organs used for breathing, the pharynx, larynx, bronchi, lungs and diaphragm. Digestive system: digestion and processing food with salivary glands, oesophagus, stomach, liver, gallbladder, pancreas, intestines, rectum and anus. Cardiovascular system (heart and circulatory system): pumping and channeling blood to and from the body and lungs with heart, blood and blood vessels. Urinary system: kidneys, ureters, bladder and urethra involved in fluid balance, electrolyte balance and excretion of urine. Integumentary system: skin, hair, fat, and nails. Skeletal system: structural support and protection with bones, cartilage, ligaments and tendons. Endocrine system: communication within the body using hormones made by endocrine glands such as the hypothalamus, pituitary gland, pineal body or pineal gland, thyroid, parathyroid and adrenals, i.e., adrenal glands. Exocrine system: various functions including lubrication and protection by exocrine glands such sweat glands, mucous glands, lacrimal glands and mammary glands Lymphatic system: structures involved in the transfer of lymph between tissues and the blood stream; includes the lymph and the nodes and vessels. The lymphatic system includes functions including immune responses and development of antibodies. Immune system: protects the organism from foreign bodies. Nervous system: collecting, transferring and processing information with brain, spinal cord, peripheral nervous system and sense organs. Sensory systems: visual system, auditory system, olfactory system, gustatory system, somatosensory system, vestibular system. Muscular system: allows for manipulation of the environment, provides locomotion, maintains posture, and produces heat. Includes skeletal muscles, smooth muscles and cardiac muscle. Reproductive system: the sex organs, such as ovaries, fallopian tubes, uterus, vagina, mammary glands, testes, vas deferens, seminal vesicles and prostate. History The notion of system (or apparatus) relies upon the concept of vital or organic function: a system is a set of organs with a definite function. This idea was already present in Antiquity (Galen, Aristotle), but the application of the term "system" is more recent. For example, the nervous system was named by Monro (1783), but Rufus of Ephesus (c. 90–120), clearly viewed for the first time the brain, spinal cord, and craniospinal nerves as an anatomical unit, although he wrote little about its function, nor gave a name to this unit. The enumeration of the principal functions - and consequently of the systems - remained almost the same since Antiquity, but the classification of them has
Biological system
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Adrenalism describes the condition of an excessive or substandard secretion of hormones related to the adrenal glands, which are found directly superior to the kidneys. Adrenalism can be further distinguished as hyperadrenalism, referring to the excessive secretion of hormones, and hypoadrenalism, referring to the insufficient secretion of hormones. The symptoms related to hyperadrenalism are known as Cushing's syndrome, and are caused by overproduction of corticosteroids, aldosterone, and androgenic steroids. Symptoms related to hypoadrenalism, such as Addison's disease, are caused by the underproductions of the hormones listed above. Furthermore, adrenalism may be caused by other external factors, which will be further discussed in the article. Etiology The adrenal glands produce important hormones that have specific roles in the homeostasis of the body, which are regulated by other glands. These hormones include aldosterone, a mineralocorticoid that regulates the amount of salt in tissue and body fluids, cortisol, a glucocorticoid that regulates metabolism and usage of macronutrients in the body, and sex hormones, such as androgens and estrogen that promote the development of secondary sex characteristics. The adrenal glands also produce epinephrine (adrenaline) and norepinephrine (noradrenaline). The production of cortisol is regulated by the hypothalamic–pituitary–adrenal axis and the hormones that are produced in the axis, namely corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH). The CRH produced by the hypothalamus stimulates the pituitary gland to produce ACTH, which stimulates the adrenal gland to produce cortisol. A negative feedback loop is formed as high levels of cortisol inhibit the hormones produced in the axis. The production of aldosterone is regulated via the renin-angiotensin II-aldosterone system, a system composed of baroreceptors and juxtaglomerular cells. Changes in the homeostasis of the human body, such as osmolality are detected by the system, which causes a chain reaction that ends with the adrenal gland either increasing or suppressing the production of aldosterone. Hyperadrenalism Hyperadrenalism refers to the overactivity of the adrenal glands. This is usually indicated by the excessive production of the hormones produced by the adrenal glands. As the hormones produced are regulated by a range of systems in the body, overactivity of the adrenal glands can be caused by different systemic dysfunctions, leading to the overproduction of specific hormones. Overproduction of Cortisol/ Hypercortisolism (HCM) When the body is exposed to an excess level of cortisol, generalized symptoms that are referred to as Cushing's syndrome appear. However, the condition may only be temporary, known as pseudo-Cushing's syndrome (PCS). Therefore, it is important to understand the cause of the syndrome to differentiate between PCS and HCM. HCM itself also has many causes, such as adrenal adenomas and carcinomas causing the adrenal gland to be unresponsive to the negative feedback loop. An increase in ACTH production could be due to a pituitary adenoma, or ectopic ACTH production, where tumors growing outside the hypothalamic-pituitary-adrenal axis also secrete ACTH. Overproduction of aldosterone/ Hyperaldosteronism The difference between primary hyperaldosteronism and secondary hyperaldosteronism lies in the causation of excess aldosterone, where primary hyperaldosteronism refers to the overproduction of aldosterone from the adrenal glands, and
Adrenalism
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Stress hormones are secreted by endocrine glands to modify one's internal environment during the times of stress. By performing various functions such as mobilizing energy sources, increasing heart rate, and downregulating metabolic processes which are not immediately necessary, stress hormones promote the survival of the organism. The secretions of some hormones are also downplayed during stress. Stress hormones include, but are not limited to: Cortisol, the main human stress hormone Catecholamines such as adrenaline and norepinephrine Vasopressin Growth hormone Role in human health Endocrine glands secrete stress hormones to modify one's internal environment during stress. By performing various functions such as mobilizing energy sources, increasing heart rate, and downregulating metabolic processes that are not immediately necessary, stress hormones promote the survival of the organism. The secretions of some hormones are also downplayed during stress. Stress hormones include, but are not limited to, cortisol, catecholamines such as adrenaline and norepinephrine, vasopressin, and growth hormone. Stress hormones play a complex role in fighting diseases and infections, as they can have both positive and negative effects on the immune system. On one hand, stress hormones can enhance the immune response by stimulating the production of cytokines, which are molecules that regulate inflammation and immunity. Stress hormones can also increase the activity of natural killer cells and macrophages, which are immune cells that can destroy infected or abnormal cells. These effects can help the body fight off acute infections, such as influenza and SARS-CoV-1 and SARS-CoV-2, which are caused by viruses. On the other hand, stress hormones can also suppress the immune response by reducing the number and function of lymphocytes, which are immune cells that produce antibodies and coordinate adaptive immunity. Stress hormones can also induce a state of chronic inflammation, which can damage the body's tissues and organs and increase the risk of chronic diseases, such as arthritis, diabetes, and cardiovascular disease. These effects can make the body more vulnerable to chronic infections, such as bacterial infections and autoimmune diseases, which are caused by the body's own immune system attacking itself. Therefore, stress hormones have a dual role in fighting diseases and infections, depending on the type, duration, and intensity of stress, as well as the nature of the pathogen. A moderate and short-term stress response can benefit the immune system, while a severe and long-term stress response can be detrimental to the immune system. The balance between the positive and negative effects of stress hormones is essential for maintaining the health and well-being of the organism. Some viruses, such as Influenza and SARS-CoV-1 and SARS-CoV-2, are known to suppress the secretion of stress hormones to avoid the organism's immune response, thus avoiding the immune protection of the organism. These viruses suppress the stress hormone cortisol by producing a protein that mimics the human ACTH hormone but is incomplete and does not have hormonal activity. ACTH is a hormone that stimulates the adrenal gland to produce cortisol and other steroid hormones. However, the organism makes antibodies against this viral protein, and those
Stress hormone
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Maternal physiological changes in pregnancy are the adaptations that take place during pregnancy that enable the accommodation of the developing embryo and fetus. These are normal physiological adaptations that cause changes in behavior, the functioning of the heart, blood vessels, and blood, metabolism including increases in blood sugar levels, kidney function, posture, and breathing. During pregnancy numerous hormones and proteins are secreted that also have a broad range of effects. Hormonal Pregnant women experience numerous adjustments in their endocrine system that help support the developing fetus. The fetal-placental unit secretes steroid hormones and proteins that alter the function of various maternal endocrine glands. Sometimes, the changes in certain hormone levels and their effects on their target organs can lead to gestational diabetes and gestational hypertension. Fetal-placental unit Levels of progesterone and estrogen rise continually throughout pregnancy, suppressing the hypothalamic axis and subsequently the menstrual cycle. The progesterone is first produced by the corpus luteum and then by the placenta in the second trimester. Women also experience increased human chorionic gonadotropin (β-hCG), which is produced by the placenta. Pancreatic insulin The placenta also produces human placental lactogen (hPL), which stimulates maternal lipolysis and fatty acid metabolism. As a result, this conserves blood glucose for use by the fetus. It can also decrease maternal tissue sensitivity to insulin, resulting in gestational diabetes. Pituitary gland The pituitary gland grows by about one-third as a result of hyperplasia of the lactrotrophs in response to the high plasma estrogen. Prolactin, which is produced by the lactrotrophs increases progressively throughout pregnancy. Prolactin mediates a change in the structure of the breast mammary glands from ductal to lobular-alveolar and stimulates milk production. Parathyroid Fetal skeletal formation and then later lactation challenges the maternal body to maintain their calcium levels. The fetal skeleton requires approximately 30 grams of calcium by the end of pregnancy. The mother's body adapts by increasing parathyroid hormone, leading to an increase in calcium uptake within the gut as well as increased calcium reabsorption by the kidneys. Maternal total serum calcium decreases due to maternal hypoalbuminemia, but the ionized calcium levels are maintained. Adrenal glands Total cortisol increases to three times of non-pregnant levels by the third trimester. The increased estrogen in pregnancy leads to increase corticosteroid-binding globulin production and in response the adrenal gland produces more cortisol. The net effect is an increase of free cortisol. This contributes to insulin resistance of pregnancy and possibly striae. Despite the increase in cortisol, the pregnant mom does not exhibit Cushing syndrome or symptoms of high cortisol. One theory is that high progesterone levels act as an antagonist to the cortisol. The adrenal gland also produces more aldosterone, leading to an eight-fold increase in aldosterone. Women do not show signs of hyperaldosterone, such as hypokalemia, hypernatremia, or high blood pressure. The adrenal gland also produces more androgens, such as testosterone, but this is buffered by estrogen's increase in sex-hormone binding globulin (SHBG). SHBG binds avidly to testosterone and to a lesser degree DHEA. Thyroid The thyroid
Maternal physiological changes in pregnancy
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Tropic hormones are hormones that have other endocrine glands as their target. Most tropic hormones are produced and secreted by the anterior pituitary. The hypothalamus secretes tropic hormones that target the anterior pituitary, and the thyroid gland secretes thyroxine, which targets the hypothalamus and therefore can be considered a tropic hormone. The term tropic is from Ancient Greek τροπικός (tropikós), in the sense "of or pertaining to a turn or change", meaning "causing a change, affecting"; this is the same origin as tropic and trope. This should not be confused with trophic, as in similar-sounding trophic hormone – the words and concepts are both unrelated. Tropic hormones are contrasted with non-tropic hormones, which directly stimulate target cells. Examples Anterior pituitary Tropic hormones from the anterior pituitary include: Thyroid-stimulating hormone (TSH or thyrotropin) – stimulates the thyroid gland to make and release thyroid hormone. Adrenocorticotropic hormone (ACTH or corticotropin) – stimulates the adrenal cortex to release glucocorticoids. Luteinizing hormone (LH) – stimulates the release of steroid hormones in gonads—the ovary and testes. Follicle-stimulating hormone (FSH) – stimulates the maturation of eggs and production of sperm. Hypothalamus In turn, the hypothalamus controls the release of hormones from the anterior pituitary by secreting a class of hypothalamic neurohormones called releasing and release-inhibiting hormones—which are released to the hypothalamo-hypophyseal portal system and act on the anterior pituitary. See also Endocrine system Non-tropic hormone Trophic hormone References Anterior pituitary hormones
Tropic hormone
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The hypothalamic–pituitary–gonadal axis (HPG axis, also known as the hypothalamic–pituitary–ovarian/testicular axis) refers to the hypothalamus, pituitary gland, and gonadal glands as if these individual endocrine glands were a single entity. Because these glands often act in concert, physiologists and endocrinologists find it convenient and descriptive to speak of them as a single system. The HPG axis plays a critical part in the development and regulation of a number of the body's systems, such as the reproductive and immune systems. Fluctuations in this axis cause changes in the hormones produced by each gland and have various local and systemic effects on the body. The axis controls development, reproduction, and aging in animals. Gonadotropin-releasing hormone (GnRH) is secreted from the hypothalamus by GnRH-expressing neurons. The anterior portion of the pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the gonads produce estrogen and testosterone. In oviparous organisms (e.g. fish, reptiles, amphibians, birds), the HPG axis is commonly referred to as the hypothalamus-pituitary-gonadal-liver axis (HPGL-axis) in females. Many egg-yolk and chorionic proteins are synthesized heterologously in the liver, which are necessary for ovocyte growth and development. Examples of such necessary liver proteins are vitellogenin and choriogenin. The HPA, HPG, and HPT axes are three pathways in which the hypothalamus and pituitary direct neuroendocrine function. Location and regulation The hypothalamus is located in the brain and secretes GnRH. GnRH travels down the anterior portion of the pituitary via the hypophyseal portal system and binds to receptors on the secretory cells of the adenohypophysis. In response to GnRH stimulation these cells produce LH and FSH, which travel into the blood stream. These two hormones play an important role in communicating to the gonads. In females FSH and LH act primarily to activate the ovaries to produce estrogen and inhibin and to regulate the menstrual cycle and ovarian cycle. Estrogen forms a negative feedback loop by inhibiting the production of GnRH in the hypothalamus. Inhibin acts to inhibit activin, which is a peripherally produced hormone that positively stimulates GnRH-producing cells. Follistatin, which is also produced in all body tissue, inhibits activin and gives the rest of the body more control over the axis. In males LH stimulates the interstitial cells located in the testicles to produce testosterone, and FSH plays a role in spermatogenesis. Only small amounts of estrogen are secreted in males. Recent research has shown that a neurosteroid axis exists, which helps the cortex to regulate the hypothalamus's production of GnRH. In addition, leptin and insulin have stimulatory effects and ghrelin has inhibitory effects on gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus. Kisspeptin also influences GnRH secretion. Function Reproduction One of the most important functions of the HPG axis is to regulate reproduction by controlling the uterine and ovarian cycles. In females, the positive feedback loop between estrogen and luteinizing hormone help to prepare the follicle in the ovary and the uterus for ovulation and implantation. When the egg is released, the empty follicle sac begins to produce progesterone to inhibit the
Hypothalamic–pituitary–gonadal axis
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The Leech Woman is a 1960 black-and-white American horror film directed by Edward Dein, produced by Joseph Gershenon, and starring Coleen Gray, Grant Williams, Gloria Talbott and Phillip Terry. The plot follows a middle-aged American woman, desperate to be young again, who uses an ancient, secret African potion to regain her lost youth and beauty. The potion works, but only temporarily, requiring repeated usage. Produced in 1959, Leech Womans US theatrical release from Universal-International was as a double feature with The Brides of Dracula. In 1997, it was featured as part of movie mocking sketch TV series Mystery Science Theater 3000s eighth season. Plot A mysterious old woman named Malla who claims to have been brought to America 140 years ago as a slave approaches endocrinologist Dr. Paul Talbot and promises to reveal to him the secret of eternal youth if he will fund her final trip back to Africa, so that she can be beautiful and young for one last night before she dies. Paul is unhappily married to the alcoholic June, who is 10 years his elder. They follow Malla to Africa and witness a secret ceremony of the Nando tribe that utilizes orchid pollen and a sacrificial male's pineal gland secretions. The secretions, extracted from the back of the neck via a special ring and mixed with the pollen, temporarily transform Malla into a young, beautiful woman. After discovering that her conniving husband only brought her along as "a guinea pig who could talk," June takes revenge, choosing Paul to be sacrificed so that she can use his pineal gland extract to become young again herself, though Malla warns her that the transformation will not last long. She steals the ring and pollen, and escapes with her jungle guide. The next morning, she finds she is old again, and kills her jungle guide for his pineal secretions. Terry makes her way back to America. Masquerading as her own niece, Terry Hart, she keeps herself young by picking up men and killing them for their pineal extract. But each time the potion wears off, she is older than she was before. As Terry, June becomes enamored of her lawyer Neil Foster, a man half her actual age. She kills his jealous fiancée Sally Howards, draining her pineal gland and eliminating Sally as competition. When the police come to investigate the murders that June has committed, she uses Sally's pineal gland extract but finds that it does not work because it is from a woman. Before the police can arrest her, she throws herself out her bedroom window, crashes to the ground and dies. When they see her body, it is much older and much more shriveled than ever. Cast Coleen Gray as June Talbot/Terry Hart Grant Williams as Neil Foster Phillip Terry as Dr. Paul Talbot Gloria Talbott as Sally Howards John van Dreelen as Bertram Garvay Estelle Helmsley as Old Malla Kim Hamilton as Young Malla Arthur Bantanides as Jerry Randall Chester Jones as Ladu (uncredited) Charles
The Leech Woman
58906
A gland is a cell or an organ in an animal's body that produces and secretes different substances either into the bloodstream or into a body cavity or outer surface that the organism needs. A gland may also function to remove unwanted substances such as urine from the body. There are two types of gland each with a different method of secretion. Endocrine glands are ductless and secrete their products, hormones, directly into interstitial spaces to be taken up into the bloodstream. Exocrine glands secrete their products through a duct into a body cavity or outer surface. Glands are mostly composed of epithelial tissue, and typically have a supporting framework of connective tissue, and a capsule. Structure Development Every gland is formed by an ingrowth from an epithelial surface. This ingrowth may in the beginning possess a tubular structure, but in other instances glands may start as a solid column of cells which subsequently becomes tubulated. As growth proceeds, the column of cells may split or give off offshoots, in which case a compound gland is formed. In many glands, the number of branches is limited, in others (salivary, pancreas) a very large structure is finally formed by repeated growth and sub-division. As a rule, the branches do not unite with one another. One exception to this rule is the liver; this occurs when a reticulated compound gland is produced. In compound glands the more typical or secretory epithelium is found forming the terminal portion of each branch, and the uniting portions form ducts and are lined with a less modified type of epithelial cell. Glands are classified according to their shape. If the gland retains its shape as a tube throughout it is termed a tubular gland. In the second main variety of gland the secretory portion is enlarged and the lumens variously increased in size. These are termed alveolar or saccular glands. Types of glands Glands are divided based on their function into two groups: Endocrine glands Endocrine glands secrete substances that circulate through the bloodstream. The glands secrete their products through basal lamina into the bloodstream. Basal lamina typically can be seen as a layer around the glands to which more than a million tiny blood vessels are attached. These glands often secrete hormones which play an important role in maintaining homeostasis. The pineal gland, thymus gland, pituitary gland, thyroid gland, and the two adrenal glands are all endocrine glands. Exocrine glands Exocrine glands secrete their products through a duct onto an outer or inner surface of the body, such as the skin or the gastrointestinal tract. Secretion is directly onto the apical surface. The glands in this group can be divided into three groups: Merocrine glands – cells secrete their substances by exocytosis. (e.g. mucous and serous glands; also called "eccrine", e.g. major sweat glands of humans, goblet cells, salivary gland, tear gland and intestinal glands) Apocrine glands – a portion of the secreting cell's body is lost during secretion. The term Apocrine gland is often
Gland
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Endocrine glands are ductless glands of the endocrine system that secrete their products, hormones, directly into the blood. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testicles, thyroid gland, parathyroid gland, hypothalamus and adrenal glands. The hypothalamus and pituitary glands are neuroendocrine organs. Pituitary gland The pituitary gland hangs from the base of the brain by the pituitary stalk, and is enclosed by bone. It consists of a hormone-producing glandular portion of the anterior pituitary and a neural portion of the posterior pituitary, which is an extension of the hypothalamus. The hypothalamus regulates the hormonal output of the anterior pituitary and creates two hormones that it exports to the posterior pituitary for storage and later release. Four of the six anterior pituitary hormones are tropic hormones that regulate the function of other endocrine organs. Most anterior pituitary hormones exhibit a diurnal rhythm of release, which is subject to modification by stimuli influencing the hypothalamus. Somatotropic hormone or growth hormone (GH) is an anabolic hormone that stimulates the growth of all body tissues especially skeletal muscle and bone. It may act directly, or indirectly via insulin-like growth factors (IGFs). GH mobilizes fats, stimulates protein synthesis, and inhibits glucose uptake and metabolism. Secretion is regulated by growth hormone-releasing hormone (GHRH) and growth hormone-inhibiting hormone (GHIH), or somatostatin. Hypersecretion causes gigantism in children and acromegaly in adults; hyposecretion in children causes pituitary dwarfism. Thyroid-stimulating hormone promotes normal development and activity of the thyroid gland. Thyrotropin-releasing hormone stimulates its release; negative feedback of thyroid hormone inhibits it. Adrenocorticotropic hormone stimulates the adrenal cortex to release corticosteroids. Adrenocorticotropic hormone release is triggered by corticotropin-releasing hormone and inhibited by rising glucocorticoid levels. The gonadotropins—follicle-stimulating hormone and luteinizing hormone regulate the functions of the gonads in both sexes. Follicle-stimulating hormone stimulates sex cell production; luteinizing hormone stimulates gonadal hormone production. Gonadotropin levels rise in response to gonadotropin-releasing hormone. Negative feedback of gonadal hormones inhibits gonadotropin release. Prolactin promotes milk production in human females. Its secretion is prompted by prolactin-releasing hormone and inhibited by prolactin-inhibiting hormone. The intermediate lobe of the pituitary gland secretes only one enzyme that is melanocyte stimulating hormone. It is linked with the formation of the black pigment in our skin called melanin. The neurohypophysis stores and releases two hypothalamic hormones: Oxytocin stimulates powerful uterine contractions, which trigger labour and delivery of an infant, and milk ejection in nursing women. Its release is mediated reflexively by the hypothalamus and represents a positive feedback mechanism. Antidiuretic hormone stimulates the kidney tubules to reabsorb and conserve water, resulting in small volumes of highly concentrated urine and decreased plasma osmolality. Antidiuretic hormone is released in response to high solute concentrations in the blood and inhibited by low solute concentrations in the blood. Hyposecretion results in diabetes insipidus. Thyroid gland The thyroid gland is located in the front of the neck, in front of the thyroid cartilage, and is shaped like a butterfly, with two wings connected by a central .
Endocrine gland
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The arcuate nucleus of the hypothalamus (also known as ARH, ARC, or infundibular nucleus) is an aggregation of neurons in the mediobasal hypothalamus, adjacent to the third ventricle and the median eminence. The arcuate nucleus includes several important and diverse populations of neurons that help mediate different neuroendocrine and physiological functions, including neuroendocrine neurons, centrally projecting neurons, and astrocytes. The populations of neurons found in the arcuate nucleus are based on the hormones they secrete or interact with and are responsible for hypothalamic function, such as regulating hormones released from the pituitary gland or secreting their own hormones. Neurons in this region are also responsible for integrating information and providing inputs to other nuclei in the hypothalamus or inputs to areas outside this region of the brain. These neurons, generated from the ventral part of the periventricular epithelium during embryonic development, locate dorsally in the hypothalamus, becoming part of the ventromedial hypothalamic region. The function of the arcuate nucleus relies on its diversity of neurons, but its central role is involved in homeostasis. The arcuate nucleus provides many physiological roles involved in feeding, metabolism, fertility, and cardiovascular regulation. Cell populations Neuroendocrine neurons Different groups of arcuate nucleus neuroendocrine neurons secrete various types or combinations of neurotransmitters and neuropeptides, such as neuropeptide Y (NPY), gonadotropin-releasing hormone (GnRH), agouti-related peptide (AgRP), cocaine- and amphetamine-regulated transcript (CART), kisspeptin, dopamine, substance P, growth hormone–releasing hormone (GHRH), neurokinin B (NKB), β-endorphin, melanocyte-stimulating hormone (MSH), and somatostatin. Proopiomelanocortin (POMC) is a precursor polypeptide that is cleaved into MSH, ACTH, and β-endorphin and expressed in the arcuate nucleus. Groups of neuroendocrine neurons include: TIDA neurons, or tuberoinfundibular dopamine neurons, are neurons that regulate the secretion of prolactin from the pituitary gland and release the neurotransmitter dopamine. TIDA neurons have nerve endings in the median eminence that release dopamine into the hypophysial portal blood. In lactating females, TIDA neurons are inhibited by the stimulus of suckling. Dopamine released from their nerve endings at the median eminence is transported to the anterior pituitary gland, where it regulates the secretion of prolactin. Dopamine inhibits prolactin secretion, so when the TIDA neurons are inhibited, there is increased secretion of prolactin, which stimulates lactogenesis (milk production). Prolactin acts in a short-loop negative feedback manner to decrease its levels by stimulating the release of dopamine. Dopaminergic neurons of the arcuate also inhibit the release of gonadotropin-releasing hormone, explaining in part why lactating (or otherwise hyperprolactinemic) women experience oligomenorrhea or amenorrhea (infrequency or absence of menses). Kisspeptin/NKB neurons within the arcuate nucleus form synaptic inputs with TIDA neurons. These neurons express estrogen receptors and also coexpress neurokinin B in female rats. GHRH neurons help to control growth hormone (GH) secretion in conjunction with somatostatin and NPY. NPY/AgRP neurons and POMC/CART neurons make up two groups of neurons in the arcuate nucleus that are centrally involved in the neuroendocrine function of feeding. Medial neurons utilize NPY peptides as neurotransmitters to stimulate appetite, and lateral neurons utilize POMC/CART to inhibit appetite. NPY and POMC/CART neurons are
Arcuate nucleus
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Breast development, also known as mammogenesis, is a complex biological process in primates that takes place throughout a female's life. It occurs across several phases, including prenatal development, puberty, and pregnancy. At menopause, breast development ceases and the breasts atrophy. Breast development results in prominent and developed structures on the chest known as breasts in primates, which serve primarily as mammary glands. The process is mediated by an assortment of hormones (and growth factors), the most important of which include estrogen, progesterone, prolactin, and growth hormone. Biochemistry Hormones The master regulators of breast development are the steroid hormones, estrogen, and progesterone, growth hormone (GH), mostly via its secretory product, insulin-like growth factor 1 (IGF-1), and prolactin. These regulators induce the expression of growth factors, such as amphiregulin, epidermal growth factor (EGF), IGF-1, and fibroblast growth factor (FGF), which in turn have specific roles in breast growth and maturation. At puberty, gonadotropin-releasing hormone (GnRH) is secreted in a pulsatile manner from the hypothalamus. GnRH induces the secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), from the pituitary gland. The secreted gonadotropins travel through the bloodstream to the ovaries and trigger the secretion of estrogen and progesterone in fluctuating amounts during each menstrual cycle. Growth hormone (GH), which is secreted from the pituitary gland, and insulin-like growth factor 1 (IGF-1), which is produced in the body in response to GH, are growth-mediating hormones. During prenatal development, infancy, and childhood, GH and IGF-1 levels are low, but progressively increase and reach a peak at puberty, with a 1.5- to 3-fold increase in pulsatile GH secretion and a 3-fold or greater increase in serum IGF-1 levels being capable of occurring at this time. In late adolescence and early adulthood, GH and IGF-1 levels significantly decrease, and continue to decrease throughout the rest of life. It has been found that both estrogen and GH are essential for breast development at puberty – in the absence of either, no development will take place. Moreover, most of the role of GH in breast development has been found to be mediated by its induction of IGF-1 production and secretion, as IGF-1 administration rescues breast development in the absence of GH. GH induction of IGF-1 production and secretion occurs in almost all types of tissue in the body, but especially in the liver, which is the source of approximately 80% of circulating IGF-1, as well as locally in the breasts. Although IGF-1 is responsible for most of the role of GH in mediating breast development, GH itself has been found to play a direct, augmenting role as well, as it increases estrogen receptor (ER) expression in breast stromal (connective) tissue, while IGF-1, in contrast, has been found to not do this. In addition to estrogen and GH/IGF-1 both being essential for pubertal breast development, they are synergistic in bringing it about. Despite the apparent necessity of GH/IGF-1 signaling in pubertal breast development however, women with Laron syndrome, in whom the growth hormone receptor (GHR) is defective
Breast development
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A lactotropic cell (also known as prolactin cell, epsilon acidophil, lactotrope, lactotroph, mammatroph, mammotroph) is a cell in the anterior pituitary which produces prolactin (a peptide hormone) in response to hormonal signals including dopamine (which is inhibitory), thyrotropin-releasing hormone and estrogen (especially during pregnancy), which are stimulatory. Prolactin is responsible for actions needed for body homeostasis, the development of breasts, and for lactation. The inhibitory effects of dopamine override the stimulatory effects of TRH in non-pregnant, non-lactating sexually mature females. Depending on the sex of the individual, lactotropic cells account for 20% - 50% of all cells in the anterior pituitary gland. The inhibitory effects of dopamine override the stimulatory effects of TRH in non-pregnant, non-lactating sexually mature females. Other regulators include oxytocin and progesterone. Males and non-pregnant, non-lactating females typically have low levels of prolactin. The number for lactotropic cells in a pregnant female will increase to allow for breast tissue development. Prolactin is involved in the maturation of mammary glands and their secretion of milk in association with oxytocin, estrogen, progesterone, glucocorticoids, and others. Prolactin has numerous other effects in both sexes. Function When lactotropic cells are observed in vitro, they are responsible for firing spontaneous action potentials, causing Ca2+ to follow the action potential pathway and allows for the exocytotic pathway, prolactin gene transcription, and hormone synthesis to remain active throughout. Prolactin gene transcription is responsible for the production of prolactin. Prolactin is involved in the maturation of mammary glands and their secretion of milk in association with oxytocin, estrogen, progesterone, glucocorticoids, and others. Prolactin has numerous other effects in both sexes. Conditions Prolactin cells are acidophilic by hematoxylin & eosin stains and, If these cells undergo neoplastic transformation, they will give rise to a prolactinoma, a prolactin-secreting pituitary adenoma. Prolactinoma is a tumor of the pituitary gland that is typically non-cancerous. This disorder is more common in females than males. Although the tumor itself may not cause symptoms, the tumor can cause an increased production of prolactin and decreased levels of estrogen and testosterone. Symptoms of both sexes could include osteoporosis, infertility, or a decrease in sexual desire. In men, prolactinoma could also cause erectile dysfunction, enlarged breast tissue, small muscles or a decrease in the amount of body hair. In women, this could cause breast discharge, irregular menstrual cycles, painful intercourse, acne, or an increase in the amount of body hair. See also Hypothalamic–pituitary–prolactin axis List of distinct cell types in the adult human body References Peptide hormone secreting cells Human cells Human female endocrine system
Lactotropic cell
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Behavioral endocrinology is a branch of endocrinology that studies the Neuroendocrine system and its effects on behavior. Behavioral endocrinology studies the biological mechanisms that produce behaviors, this gives insight into the evolutionary past. The field has roots in ethology, endocrinology and psychology. The neuroendocrine system The neuroendocrine system is an integrated system composed of neurons, glands and non-endocrine tissues, and the hormones and neurochemicals they produce and receive collectively regulate physiological or behavioral state. Hypothalamus The hypothalamus is a distinct part of the brain that is made up of neurons and its main purpose is to maintain homeostasis. The hypothalamus also plays an important part in survival of the individual by integrating the interactions between hormonal and behavioral processes, such as, eating behavior and aggressive behavior. Pituitary gland The pituitary gland located in the brain is a major system in neuroendocrine system because the secretion of hormones from the anterior pituitary is directly regulated by the central nervous system. Neuroendocrine regulation of behavior Social behavior, reproductive behavior, moods, feelings, attitudes, development and survival are affected by the neuroendocrine system and studied in the field of behavioral endocrinology. Adrenal Hormones Cortisol See the Cortisol: Memory and Stress sections for more information on how cortisol has been found to affect behavior. Adrenaline See the Adrenaline: Emotional response and Memory sections for more information on how adrenaline affects behavior. Sex Steroids Testosterone Testosterone is secreted by the testicles of males and the ovaries of females, although small amounts are also secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid. See Testosterone: Aggression and criminality and Testosterone: Brain for more information on how testosterone effects behavior. Estrogen Estrogens, together, make up a group of primary female sex hormones synthesized in the ovaries. See Estrogen: Brain and behavior for more on the role of estrogen in behavioral endocrinology. Thyroid Hormones Thyroid hormones are responsible for controlling metabolism, nervous system, body temperature and development of several organ systems such as the reproductive system. Diseases and medicine Hyperthyroidism and hypothyroidism are the two major dysfunctions associated to behavioral and brain chemistry changes due to the imbalances in the thyroid hormones, triiodothyronine (T3) and thyroxine (T4). History Behavioral endocrinology has roots in ethology and is also seen as a combination of endocrinology and psychology. Like ethology, behavioral endocrinology focuses on behavior on the level of the whole organism. The invention of radioimmunoassay techniques revolutionized behavioral endocrinology, allowing scientists to see and quantify hormones. The field historically resists reductionist thinking and focuses on the physiological aspects of behavior. Influential scientists Charles Otis Whitman Karl Lashley Organizations Society of Behavioral Neuroendocrinology- Platform that provides a network between interested persons from all different experience levels. See also Neuroendocrinology Endocrinology Hormone Behavior Endocrine disease Neuroendocrine cell Evolutionary psychology References Endocrinology
Behavioral endocrinology
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The paraventricular nucleus (PVN, PVA, or PVH) is a nucleus in the hypothalamus. Anatomically, it is adjacent to the third ventricle and many of its neurons project to the posterior pituitary. These projecting neurons secrete oxytocin and a smaller amount of vasopressin, otherwise the nucleus also secretes corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH). CRH and TRH are secreted into the hypophyseal portal system and act on different targets neurons in the anterior pituitary. PVN is thought to mediate many diverse functions through these different hormones, including osmoregulation, appetite, and the response of the body to stress. Location The paraventricular nucleus lies adjacent to the third ventricle. It lies within the periventricular zone and is not to be confused with the periventricular nucleus, which occupies a more medial position, beneath the third ventricle. The PVN is highly vascularised and is protected by the blood–brain barrier, although its neuroendocrine cells extend to sites (in the median eminence and in the posterior pituitary) beyond the blood–brain barrier. Neurons The PVN contains magnocellular neurosecretory cells whose axons extend into the posterior pituitary, parvocellular neurosecretory cells that project to the median eminence, ultimately signalling to the anterior pituitary, and several populations of other cells that project to many different brain regions including parvocellular preautonomic cells that project to the brainstem and spinal cord. Magnocellular neurosecretory neurons The magnocellular cells in the PVN elaborate and secrete two peptide hormones: oxytocin and vasopressin. These hormones are packaged into large vesicles, which are then transported down the unmyelinated axons of the cells and released from neurosecretory nerve terminals residing in the posterior pituitary gland. Similar magnocellular neurons are found in the supraoptic nucleus which also secrete vasopressin and a smaller amount of oxytocin. Parvocellular neurosecretory neurons The axons of the parvocellular neurosecretory neurons of the PVN project to the median eminence, a neurohemal organ at the base of the brain, where their neurosecretory nerve terminals release their hormones at the primary capillary plexus of the hypophyseal portal system. The median eminence contains fiber terminals from many hypothalamic neuroendocrine neurons, secreting different neurotransmitters or neuropeptides, including vasopressin, corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH), gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GHRH), dopamine (DA) and somatostatin (growth hormone release inhibiting hormone, GIH) into blood vessels in the hypophyseal portal system. The blood vessels carry the peptides to the anterior pituitary gland, where they regulate the secretion of hormones into the systemic circulation. The parvocellular neurosecretory cells include those that make: Corticotropin-releasing hormone (CRH), which regulates ACTH secretion from the anterior pituitary gland Vasopressin, which also regulates ACTH secretion (vasopressin and CRH act synergistically to stimulate ACTH secretion) Thyrotropin-releasing hormone (TRH), which regulates TSH and prolactin secretion Centrally-projecting neurons As well as neuroendocrine neurons, the PVN contains interneurons and populations of neurons that project centrally (i.e., to other brain regions). The centrally-projecting neurons include Parvocellular oxytocin cells, which project mainly to the brainstem and spinal cord. These neurons are thought to have a role in gastric reflexes and penile erection, Parvocellular
Paraventricular nucleus of hypothalamus
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Hypothalamic–pituitary hormones are hormones that are produced by the hypothalamus and pituitary gland. Although the organs in which they are produced are relatively small, the effects of these hormones cascade throughout the body. They can be classified as a hypothalamic–pituitary axis (HP axis) of which the adrenal (), gonadal (), thyroid (), somatotropic (), and prolactin () axes are branches. It is possible for the function of these hormones to be altered by physical activity. In posterior pituitary we have hormones that control absorption of water and oxytocin. Anterior hypophysis, neurosecretory cells which release hormones. There is a pituitary portal system, with which the hormones are transported. These hormones are prolactin, growth hormone, TSH, adrenocorticotropic hormone, FSH and LH. They are all released by anterior pituitary. Some have targets in glands and some with direct function. Anterior pituitary is an amalgam of hormone producing glandular cells. There are conditions related to the limbic system which regulate the hormone release. And also thalamus, with pain. Many of these stimuli come from the senses of the subject. The temperature control can be found in the hypothalamus. There is also regulation of water balance. And also hunger, and also something associated with water balance control (ADH). · Corticotropic releasing hormone CRH: stimulates ACTH secretion · Thyrotropin releasing hormone (TRH): stimulates TSH and prolactin secretion · Growth hormone releasing hormone (GHRH): stimulates GH secretion · Somatostatin: inhibits GH (and other hormone) secretion · Gonadotropin releasing hormone (GnRH): stimulates FSH and LH secretion · Prolactin releasing hormone (PRH): stimulates PRL secretion · Prolactin inhibiting hormone (dopamine): inhibits PRL secretion These hypothalamic hormones are secreted in pulse. They act on specific membrane receptors. They are glycoproteins. Then you have the signal. They stimulate release of pituitary hormones. They stimulate synthesis of pituitary hormones, stimulate release stored pituitary hormones, stimulate hyperplasia and hypertrophy of target cells and regulate their own receptors. Anterior pituitary produces prolactin, GH, TSH, ACTH, FSH, LH. 15–20% of corticotroph cells, produce ACTH. The targets are the adrenal glands, adipocytes and melanocytes. 3–5% thyrotroph cells, produce TSH. 10–15%, Gonadotroph, produce LH and FSH 40–50% somatotroph, produce GH in particular in childhood. 10–15% lactotroph, produce prolactin. References Hormones of the hypothalamus Hormones of the pituitary gland Hormones of the hypothalamus-pituitary axis
Hypothalamic–pituitary hormone
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The hypothalamic–pituitary–thyroid axis (HPT axis for short, a.k.a. thyroid homeostasis or thyrotropic feedback control) is part of the neuroendocrine system responsible for the regulation of metabolism and also responds to stress. As its name suggests, it depends upon the hypothalamus, the pituitary gland, and the thyroid gland. The hypothalamus senses low circulating levels of thyroid hormone (Triiodothyronine (T3) and Thyroxine (T4)) and responds by releasing thyrotropin-releasing hormone (TRH). The TRH stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH). The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland. The HPA, HPG, and HPT axes are three pathways in which the hypothalamus and pituitary direct neuroendocrine function. Physiology Thyroid homeostasis results from a multi-loop feedback system that is found in virtually all higher vertebrates. Proper function of thyrotropic feedback control is indispensable for growth, differentiation, reproduction and intelligence. Very few animals (e.g. axolotls and sloths) have impaired thyroid homeostasis that exhibits a very low set-point that is assumed to underlie the metabolic and ontogenetic anomalies of these animals. The pituitary gland secretes thyrotropin (TSH; Thyroid Stimulating Hormone) that stimulates the thyroid to secrete thyroxine (T4) and, to a lesser degree, triiodothyronine (T3). The major portion of T3, however, is produced in peripheral organs, e.g. liver, adipose tissue, glia and skeletal muscle by deiodination from circulating T4. Deiodination is controlled by numerous hormones and nerval signals including TSH, vasopressin and catecholamines. Both peripheral thyroid hormones (iodothyronines) inhibit thyrotropin secretion from the pituitary (negative feedback). Consequently, equilibrium concentrations for all hormones are attained. TSH secretion is also controlled by thyrotropin releasing hormone (thyroliberin, TRH), whose secretion itself is again suppressed by plasma T4 and T3 in CSF (long feedback, Fekete–Lechan loop). Additional feedback loops are ultrashort feedback control of TSH secretion (Brokken-Wiersinga-Prummel loop) and linear feedback loops controlling plasma protein binding. Recent research suggested the existence of an additional feedforward motif linking TSH release to deiodinase activity in humans. The existence of this TSH-T3 shunt could explain why deiodinase activity is higher in hypothyroid patients and why a minor fraction of affected individuals may benefit from substitution therapy with T3. Convergence of multiple afferent signals in the control of TSH release including but not limited to T3, cytokines and TSH receptor antibodies may be the reason for the observation that the relation between free T4 concentration and TSH levels deviates from a pure loglinear relation that has previously been proposed. Recent research suggests that ghrelin also plays a role in the stimulation of T4 production and the subsequent suppression of TSH directly and by negative feedback. Functional states of thyrotropic feedback control Euthyroidism: Normal thyroid function Hypothyroidism: Reduced thyroid function primary hypothyroidism: Feedback loop interrupted by low thyroid secretory capacity, e.g. after thyroid surgery or in case of autoimmune thyroiditis secondary hypothyroidism: Feedback loop
Hypothalamic–pituitary–thyroid axis
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A parietal eye, also known as a third eye or pineal eye, is a part of the epithalamus present in some vertebrates. The eye is located at the top of the head, is photoreceptive and is associated with the pineal gland, regulating circadian rhythmicity and hormone production for thermoregulation. The hole in the head which contains the eye is known as a pineal foramen or parietal foramen, since it is often enclosed by the parietal bones. The parietal eye was discovered by Franz Leydig in 1872 from lizards. Discovery Franz Leydig, professor of zoology at the University of Tübingen, dissected four species of European lizards – the slow worm (Anguis fragilis) and three species of Lacerta– in 1872, and found cup-like protrusions under the middle portion of their brains. He believed these to be glandular in nature, and gave them the name frontal organ (German Stirnorgan). In 1886, University of Oxford anatomist Walter Baldwin Spencer reported his dissection results of 29 species of lizards, and noted the presence of the same structure Leydig had described. He called it the pineal eye or parietal eye, as he saw it was associated with the parietal foramen and the pineal stalk. In 1918, Swedish zoologist Nils Holmgren found the pineal eye in frogs and dogfish. He noted that the structure contained sensory cells that looked like the cone cells of the retina, and hypothesised that this pineal eye could be a primitive light-sensing organ (photoreceptor). The organ has become popularly known as the "third eye". Presence in various animals The parietal eye is found in the tuatara, most lizards, frogs, salamanders, certain bony fish, sharks, and lampreys. It is absent in mammals, but was present in their closest extinct relatives, the therapsids, suggesting it was lost during the course of the mammalian evolution due to it being useless in endothermic animals. It is also absent in the ancestrally endothermic ("warm-blooded") archosaurs such as birds. The parietal eye is also lost in ectothermic ("cold-blooded") archosaurs like crocodilians, and in turtles, which may be grouped with archosaurs in Archelosauria. Despite being lepidosaurs, as lizards and tuatara are, snakes lack a parietal eye. Anatomy The third eye, where present, is always much smaller than the main paired eyes, and, in living species, it is always covered by skin, and is usually not readily visible externally. The parietal eye is a part of the epithalamus, which can be divided into two major parts; the epiphysis (the pineal organ, or pineal gland if mostly endocrine) and the parapineal organ (often called the parietal eye, or if it is photoreceptive, the third eye). These structures arise as a single anterior evagination of the pineal organ or as a separate outgrowth of the roof of the diencephalon, but during development it divides into two more or less bilaterally symmetric organs which rotate their location to become a caudal pineal organ and a parapineal organ. In some species, it protrudes through the skull. The parietal eye uses a different biochemical method
Parietal eye
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APUD cells (DNES cells) constitute a group of apparently unrelated endocrine cells, which were named by the scientist A.G.E. Pearse, who developed the APUD concept in the 1960s based on calcitonin-secreting parafollicular C cells of dog thyroid. These cells share the common function of secreting a low molecular weight polypeptide hormone. There are several different types which secrete the hormones secretin, cholecystokinin and several others. The name is derived from an acronym, referring to the following: Amine Precursor Uptake – for high uptake of amine precursors including 5-hydroxytryptophan (5-HTP) and dihydroxyphenylalanine (DOPA). Decarboxylase – for high content of the enzyme amino acid decarboxylase (for conversion of precursors to amines). Cells in APUD system Adenohypophysis Neurons of Hypothalamus Chief Cells of Parathyroid Adrenal Medullary Cells Glomus cells in Carotid Body Melanocytes of Skin Cells of Pineal Gland Renin producing cells in the kidney See also Apudoma Enteroendocrine cell Neuroendocrine cell List of human cell types derived from the germ layers References External links Endocrine cells
APUD cell
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Neuroendocrinology is the branch of biology (specifically of physiology) which studies the interaction between the nervous system and the endocrine system; i.e. how the brain regulates the hormonal activity in the body. The nervous and endocrine systems often act together in a process called neuroendocrine integration, to regulate the physiological processes of the human body. Neuroendocrinology arose from the recognition that the brain, especially the hypothalamus, controls secretion of pituitary gland hormones, and has subsequently expanded to investigate numerous interconnections of the endocrine and nervous systems. The endocrine system consists of numerous glands throughout the body that produce and secrete hormones of diverse chemical structure, including peptides, steroids, and neuroamines. Collectively, hormones regulate many physiological processes. The neuroendocrine system is the mechanism by which the hypothalamus maintains homeostasis, regulating reproduction, metabolism, eating and drinking behaviour, energy utilization, osmolarity and blood pressure. Neuroendocrine system Hypothalamus The hypothalamus is commonly known as the relay center of the brain because of its role in integrating inputs from all areas of the brain and producing a specific response. In the neuroendocrine system, the hypothalamus receives electrical signals from different parts of the brain and translates those electrical signals into chemical signals in the form of hormones or releasing factors. These chemicals are then transported to the pituitary gland and from there to the systemic circulation. Pituitary gland The pituitary gland is divided into three lobes: the anterior pituitary, the intermediate pituitary lobe, and the posterior pituitary. The hypothalamus controls the anterior pituitary's hormone secretion by sending releasing factors, called tropic hormones, down the hypothalamo-hypophysial portal system. For example, thyrotropin-releasing hormone released by the hypothalamus in to the portal system stimulates the secretion of thyroid-stimulating hormone by the anterior pituitary. The posterior pituitary is directly innervated by the hypothalamus; the hormones oxytocin and vasopressin are synthesized by neuroendocrine cells in the hypothalamus and stored at the nerve endings in the posterior pituitary. They are secreted directly into systemic circulation by the hypothalamic neurons. Major neuroendocrine axes Oxytocin and vasopressin (also called anti-diuretic hormone), the two neurohypophysial hormones of the posterior pituitary gland (the neurohypophysis), are secreted from the nerve endings of magnocellular neurosecretory cells into the systemic circulation. The cell bodies of the oxytocin and vasopressin neurons are in the paraventricular nucleus and supraoptic nucleus of the hypothalamus, respectively, and the electrical activity of these neurons is regulated by afferent synaptic inputs from other brain regions. By contrast, the hormones of the anterior pituitary gland (the adenohypophysis) are secreted from endocrine cells that, in mammals, are not directly innervated, yet the secretion of these hormones (adrenocorticotrophic hormone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, prolactin, and growth hormone) remains under the control of the hypothalamus. The hypothalamus controls the anterior pituitary gland via releasing factors and release-inhibiting factors; these are substances released by hypothalamic neurons into blood vessels at the base of the brain, at the median eminence. These vessels, the hypothalamo-hypophysial portal vessels, carry the hypothalamic factors to the anterior pituitary, where they bind to
Neuroendocrinology
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Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, genetic disorders, radiation, surgery, head trauma, lesion, tumour or other physical injury to the hypothalamus. The hypothalamus is the control center for several endocrine functions. Endocrine systems controlled by the hypothalamus are regulated by antidiuretic hormone (ADH), corticotropin-releasing hormone, gonadotropin-releasing hormone, growth hormone-releasing hormone, oxytocin, all of which are secreted by the hypothalamus. Damage to the hypothalamus may impact any of these hormones and the related endocrine systems. Many of these hypothalamic hormones act on the pituitary gland. Hypothalamic disease therefore affects the functioning of the pituitary and the target organs controlled by the pituitary, including the adrenal glands, ovaries and testes, and the thyroid gland. Numerous dysfunctions manifest as a result of hypothalamic disease. Damage to the hypothalamus may cause disruptions in body temperature regulation, growth, weight, sodium and water balance, milk production, emotions, and sleep cycles. Hypopituitarism, neurogenic diabetes insipidus, tertiary hypothyroidism, and developmental disorders are examples of precipitating conditions caused by hypothalamic disease. Hypopituitarism The hypothalamus and pituitary gland are tightly integrated. Damage to the hypothalamus will impact the responsiveness and normal functioning of the pituitary. Hypothalamic disease may cause insufficient or inhibited signalling to the pituitary leading to deficiencies of one or more of the following hormones: thyroid-stimulating hormone, adrenocorticotropic hormone, beta-endorphin, luteinizing hormone, follicle-stimulating hormone, and melanocyte–stimulating hormones. Treatment for hypopituitarism involves hormone replacement therapy. Neurogenic diabetes insipidus Neurogenic diabetes insipidus may occur due to low levels of ADH production from the hypothalamus. Insufficient levels of ADH result in increased thirst and urine output, and prolonged excessive urine excretion increases the risk of dehydration. Tertiary hypothyroidism The thyroid gland is an auxiliary organ to the hypothalamus-pituitary system. Thyrotropin-releasing hormone (TRH) produced by the hypothalamus signals to the pituitary to release thyroid-stimulating hormone (TSH), which then stimulates the thyroid to secrete T4 and T3 thyroid hormones. Secondary hypothyroidism occurs when TSH secretion from the pituitary is impaired, whereas tertiary hypothyroidism is the deficiency or inhibition of TRH. Thyroid hormones are responsible for metabolic activity. Insufficient production of the thyroid hormones result in suppressed metabolic activity and weight gain. Hypothalamic disease may therefore have implications for obesity. Developmental disorders Growth hormone-releasing hormone (GHRH) is another releasing factor secreted by the hypothalamus. GHRH stimulates the pituitary gland to secrete growth hormone (GH), which has various effects on body growth and sexual development. Insufficient GH production may cause poor somatic growth, precocious puberty or gonadotropin deficiency, failure to initiate or complete puberty, and is often associated with rapid weight gain, low T4, and low levels of sex hormones. Sleep disorders Non-24-hour sleep-wake syndrome, a disabling condition in which one's sleep/wake cycle is longer, or rarely, shorter, than the standard 24 hours, is thought to involve or be caused by, at least in some cases, an abnormal functioning of the suprachiasmatic nucleus (SCN) in the hypothalamus. References External links Hypothalamus disorders
Hypothalamic disease
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The following is a partial list of the "A" codes for Medical Subject Headings (MeSH), as defined by the United States National Library of Medicine (NLM). This list continues the information at List of MeSH codes (A05). Codes following these are found at List of MeSH codes (A07). For other MeSH codes, see List of MeSH codes. The source for this content is the set of 2006 MeSH Trees from the NLM. – endocrine system – chromaffin system – chromaffin cells – chromaffin granules – enterochromaffin cells – enterochromaffin-like cells – para-aortic bodies – paraganglia, chromaffin – enteroendocrine cells – enterochromaffin cells – enterochromaffin-like cells – gastrin-secreting cells – glucagon-secreting cells – insulin-secreting cells – pancreatic polypeptide-secreting cells – somatostatin-secreting cells – endocrine glands – adrenal glands – adrenal cortex – zona fasciculata – zona glomerulosa – zona reticularis – adrenal medulla – gonads – ovary – corpus luteum – luteal cells – ovarian follicle – follicular fluid – granulosa cells – theca cells – testis – leydig cells – islets of langerhans – glucagon-secreting cells – insulin-secreting cells – pancreatic polypeptide-secreting cells – somatostatin-secreting cells – parathyroid glands – pineal gland – pituitary-adrenal system – pituitary gland – pituitary gland, anterior – pituitary gland, posterior – thyroid gland – neurosecretory systems – hypothalamo-hypophyseal system – median eminence – pituitary gland – pituitary gland, anterior – pituitary gland, posterior – pineal gland The list continues at List of MeSH codes (A07). A06
List of MeSH codes (A06)
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The hypothalamic–pituitary–adrenal axis (HPA axis or HTPA axis) is a complex set of direct influences and feedback interactions among three components: the hypothalamus (a part of the brain located below the thalamus), the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal (also called "suprarenal") glands (small, conical organs on top of the kidneys). These organs and their interactions constitute the HPA axis. The HPA axis is a major neuroendocrine system that controls reactions to stress and regulates many body processes, including digestion, immune responses, mood and emotions, sexual activity, and energy storage and expenditure. It is the common mechanism for interactions among glands, hormones, and parts of the midbrain that mediate the general adaptation syndrome (GAS). While steroid hormones are produced mainly in vertebrates, the physiological role of the HPA axis and corticosteroids in stress response is so fundamental that analogous systems can be found in invertebrates and monocellular organisms as well. The HPA axis, hypothalamic–pituitary–gonadal (HPG) axis, hypothalamic–pituitary–thyroid (HPT) axis, and the hypothalamic–neurohypophyseal system are the four major neuroendocrine systems through which the hypothalamus and pituitary direct neuroendocrine function. Anatomy The key elements of the HPA axis are: The paraventricular nucleus of the hypothalamus: It contains neuroendocrine neurons which synthesize and secrete vasopressin and corticotropin-releasing hormone (CRH). The anterior lobe of the pituitary gland: CRH and vasopressin stimulate the anterior lobe of pituitary gland to secrete adrenocorticotropic hormone (ACTH), once known as corticotropin. The adrenal cortex: It produces glucocorticoid hormones (mainly cortisol in humans) in response to stimulation by ACTH. Glucocorticoids in turn, act back on the hypothalamus and pituitary (to suppress CRH and ACTH production) in a negative feedback cycle. CRH and vasopressin are released from neurosecretory nerve terminals at the median eminence. CRH is transported to the anterior pituitary through the portal blood vessel system of the hypophyseal stalk and vasopressin is transported by axonal transport to the posterior pituitary gland. There, CRH and vasopressin act synergistically to stimulate the secretion of stored ACTH from corticotrope cells. ACTH is transported by the blood to the adrenal cortex of the adrenal gland, where it rapidly stimulates the biosynthesis of corticosteroids such as cortisol from cholesterol. Cortisol is a major stress hormone and has effects on many tissues in the body, including the brain. In the brain, cortisol acts on two types of receptors: mineralocorticoid receptors and glucocorticoid receptors, and these are expressed by many different types of neurons. One important target of glucocorticoids is the hypothalamus, which is a major controlling centre of the HPA axis. Vasopressin can be thought of as "water conservation hormone" and is also known as "antidiuretic hormone(ADH)". It is released when the body is dehydrated and has potent water-conserving effects on the kidney. It is also a potent vasoconstrictor. Important to the function of the HPA axis are some of the following feedback loops: Cortisol produced in the adrenal cortex will negatively feedback to inhibit both the hypothalamus and the pituitary gland. This reduces the secretion of CRH and
Hypothalamic–pituitary–adrenal axis
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Hypothalamic-pituitary axis Hypothalamus Pineal body (epiphysis) Pituitary gland (hypophysis) The pituitary gland (or hypophysis) is an endocrine gland about the size of a pea and weighing in humans. It is a protrusion off the bottom of the hypothalamus at the base of the brain, and rests in a small, bony cavity (sella turcica) covered by a dural fold (diaphragma sellae). The pituitary is functionally connected to the hypothalamus by the median eminence via a small tube called the infundibular stem or pituitary stalk. The anterior pituitary (adenohypophysis) is connected to the hypothalamus via the hypothalamo–hypophyseal portal vessels, which allows for quicker and more efficient communication between the hypothalamus and the pituitary. Anterior pituitary lobe (adenohypophysis) Posterior pituitary lobe (neurohypophysis) Oxytocin and anti-diuretic hormone are not secreted in the posterior lobe, merely stored. Thyroid Digestive system Stomach Duodenum (small intestine) Liver Pancreas The pancreas is a heterocrine gland as it functions both as an endocrine and as an exocrine gland. Kidney Adrenal glands Adrenal cortex Adrenal medulla Reproductive Testes Ovarian follicle and corpus luteum Placenta (when pregnant) Uterus (when pregnant) Calcium regulation Parathyroid Skin Other Heart Bone Skeletal muscle In 1998, skeletal muscle was identified as an endocrine organ due to its now well-established role in the secretion of myokines. The use of the term myokine to describe cytokines and other peptides produced by muscle as signalling molecules was proposed in 2003. Adipose tissue Signalling molecules released by adipose tissue are referred to as adipokines. References Endocrine system Human physiology endocrine organs
List of human endocrine organs and actions
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An antithyroid agent is a hormone inhibitor acting upon thyroid hormones. The main antithyroid drugs are carbimazole (in the UK), methimazole (in the US), and propylthiouracil (PTU). A less common antithyroid agent is potassium perchlorate. Classification based on mechanisms of action The mechanisms of action of antithyroid drugs are not completely understood. Based on their mechanisms of action, the drugs are classified into following six classes. Thyroid hormone synthesis inhbitors These drugs probably inhibit the enzyme thyroid peroxidase ( thyroperoxidase), decreasing iodide oxidation, iodination of tyrosyl residues in thyroglobulin, and coupling of iodotyrosyl and iodothyronyl residues. It is thought that they inhibit the thyroperoxidase-catalyzed oxidation reactions by acting as substrates for the postulated peroxidase-iodine complex, thus competitively inhibiting the interaction with the amino acid tyrosine. The most common drugs in this class are thioamides, which include propylthiouracil, methimazole and its prodrug carbimazole. Additionally, propylthiouracil may reduce the de-iodination of thyroxine (tetraiodothyronine; T4) into triiodothyronine (T3) in peripheral tissues. Lugol's iodine is used to temporarily block thyroid hormone synthesis before surgeries. It is also used to treat patients with thyroid storm or, more commonly, to reduce thyroid vascularity before thyroidectomy (surgical removal of the thyroid gland). Iodide uptake inhibitors They decrease uptake of iodide ions (I−) into follicular cells of the thyroid gland. Since their molecules have structural similarities with the iodide ion, they compete with iodide for being transported by the sodium/iodide symporter, which is a transporter protein that co-transports Na+ and I− ions. Iodide transport is a key step in the biosynthesis of the thyroid hormones T4 and T3. For example, potassium perchlorate competitively inhibits the active iodide transport mechanism in the thyroid gland, which has the capacity to selectively concentrate iodide against a large concentration gradient. Besides perchlorates, other examples of iodide uptake inhibitors include pertechnetates, thiocyanates, nitrates. These drugs are no longer used due to high toxicity and adverse effects. Thyroid hormone release inhibitors They inhibit release (secretion) of thyroid hormones by the thyroid gland. The most studied drug in this class is lithium, which inhibits thyroid hormone secretion by inhibiting iodotyrosine coupling, thyroidal iodide uptake, and alteration in structure of thyroglobulin, a protein which acts as a substrate for the synthesis of thyroid hormones and storage of inactive forms of T3, T4 and iodine within the lumen of thyroid follicular cells. Since lithium is neither metabolized nor protein-bound, its bioavailability usually is close to 100%. Hence, there are risks of serious side effects such as lithium toxicity, hypothyroidism, and diabetes insipidus. Excess iodine Excessive iodine intake can temporarily inhibit production of thyroid hormones. This occurs because of the Wolff-Chaikoff effect, which is a phenomenon of rejection of large quantities of iodine by the thyroid gland, therefore preventing it from synthesizing large quantities of thyroid hormones. Iodine radiopharmaceuticals They are radioisotopes of iodine. In small doses, when they are taken up by overactive thyroid follicular cells, they emit small amounts of beta radiation that destroys not all, but many thyroid follicular cells, thereby reducing thyroid hormone production.
Antithyroid agent
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Releasing hormones and inhibiting hormones are hormones whose main purpose is to control the release of other hormones, either by stimulating or inhibiting their release. They are also called liberins () and statins () (respectively), or releasing factors and inhibiting factors. The principal examples are hypothalamic-pituitary hormones that can be classified from several viewpoints: they are hypothalamic hormones (originating in the hypothalamus), they are hypophysiotropic hormones (affecting the hypophysis, that is, the pituitary gland), and they are tropic hormones (having other endocrine glands as their target). For example, thyrotropin-releasing hormone (TRH) is released from the hypothalamus in response to low levels of secretion of thyroid-stimulating hormone (TSH) from the pituitary gland. The TSH in turn is under feedback control by the thyroid hormones T4 and T3. When the level of TSH is too high, they feed back on the brain to shut down the secretion of TRH. Synthetic TRH is also used by physicians as a test of TSH reserve in the pituitary gland as it should stimulate the release of TSH and prolactin from this gland. The main releasing hormones are as follows: The hypothalamus uses thyrotropin-releasing hormone (TRH or thyroliberin) to tell the pituitary to release thyrotropin. The hypothalamus uses corticotropin-releasing hormone (CRH or corticoliberin) to tell the pituitary to release corticotropin. The hypothalamus uses gonadotropin-releasing hormone (GnRH or gonadoliberin) to tell the pituitary to release gonadotropin. The hypothalamus uses growth hormone–releasing hormone (GHRH or somatoliberin) to tell the pituitary to release somatotropin. The main release-inhibiting hormones or inhibiting hormones are as follows: The hypothalamus uses somatostatin to tell the pituitary to inhibit somatotropin and to tell the gastrointestinal tract to inhibit various gastrointestinal hormones. There are various other inhibiting factors that also have tropic endocrine inhibition activity. Such activity is only one of many functions that they have (such as neurotransmitter and receptor antagonist roles), and they are not always called hormones, although many are neuropeptides or neurosteroids. They include the following: The hypothalamus uses dopamine as a prolactostatin to tell the pituitary to inhibit prolactin; it is also created elsewhere in the brain and the adrenal cortex as a neurotransmitter to affect many other systems. The hypothalamus uses RFRP-3 in mammals or GnIH in avian species to inhibit GnRH. The hypothalamus uses follistatin to tell the pituitary to inhibit follicle-stimulating hormone; it also has many other systemic effects. Myocytes use myostatin to tell each other to inhibit myogenesis. Melanocyte-inhibiting factor (melanostatin) inhibits release of other neuropeptides such as alpha-MSH and also has many other functions. There is a neuropeptide called cortistatin and a class of steroidal cortistatins. Examples of releasing and inhibiting hormones for exocrine hormones are gastrin-releasing peptide (GRP) and gastric inhibitory polypeptide (GIP), which regulate gastrin production. Mechanism Releasing hormones increase (or, in case of inhibitory factors, decrease) the intracellular concentration of calcium (Ca2+), resulting in vesicle fusion of the respective primary hormone. For GnRH, TRH and GHRH the increase in Ca2+ is achieved by the releasing hormone coupling and activating G protein coupled
Releasing and inhibiting hormones
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Somatotropes (from the Greek sōmat meaning "body" and tropikós meaning "of or pertaining to a turn or change") are cells in the anterior pituitary that produce growth hormone. Structure Somatotropic cells constitute about 30−40% of anterior pituitary cells. They release growth hormone (GH) in response to Growth hormone releasing hormone (GHRH, or somatocrinin) or are inhibited by GHIH (somatostatin), both received from the hypothalamus via the hypophyseal portal system vein and the secondary plexus. Clinical significance Hormone deficiency When levels of somatotropin are low in the body, a physician may prescribe human growth hormone as a drug. Deficiency in somatotrope secretion before puberty or before the end of new bone tissue growth, can lead to pituitary dwarfism. When growth hormone is deficient, blood sugar is low because insulin is not opposed by normal amount of growth hormone. Hormone excess If there is an excess of growth hormone, it is usually because of over-secretion of somatotrope cells in the anterior pituitary gland. A significant amount of excess somatotrope secretion before puberty or before the end of new bone tissue growth can lead to gigantism, a disease that causes excess growth of body (e.g. being over 7 ft. tall) and unusually long limbs. An excess of secretion of growth hormone after puberty can lead to acromegaly. This is a disease that causes abnormal growth in the hands, head, jaw, and tongue. Some symptoms associated with acromegaly include heavy sweating, oily skin, improper processing of sugars in the diet (diabetes), high blood pressure, increased calcium in urine and swelling of the thyroid gland and arthritis. Other animals Bovine somatotropin occurs in the pituitary of cattle and differs in structure from human pituitary growth hormone and is biologically inactive in the human being. Bovine somatotropin aids in regulating the amount of milk produced. Recombinant bovine somatotropin (rBST) is a hormone that is injected in cows that increases milk production. See also Hypothalamic–pituitary–somatic axis List of human cell types derived from the germ layers List of distinct cell types in the adult human body References Peptide hormone secreting cells Human cells
Somatotropic cell
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A pineal gland cyst is a usually benign (non-malignant) cyst in the pineal gland, a small endocrine gland in the brain. Historically, these fluid-filled bodies appeared on of magnetic resonance imaging (MRI) brain scans, but were more frequently diagnosed at death, seen in of autopsies. A 2007 study by Pu et al. found a frequency of 23% in brain scans (with a mean diameter of 4.3 mm). Despite the pineal gland being in the center of the brain, due to recent advancements in endoscopic medicine, endoscopic brain surgery to drain and/or remove the cyst can be done with the patient spending 5-10 nights in the hospital, and being fully recovered in weeks, rather than a year, as is the case with open-skull brain surgery. The National Organization for Rare Disorders states that pineal cysts larger than 5.0 mm are "rare findings" and are possibly symptomatic. If narrowing of the cerebral aqueduct occurs, many neurological symptoms may exist, including headaches, vertigo, nausea, muscle fasciculations, eye sensitivity, and ataxia. Continued monitoring of the cyst might be recommended to monitor its growth, and surgery may be necessary. Additional images References Further reading External links Pineal Cyst Images and Radiological Findings radiopaedia.org article - Pineal Cyst Central nervous system disorders Neuroendocrinology Cysts
Pineal gland cyst
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Sheehan's syndrome, also known as postpartum pituitary gland necrosis, occurs when the pituitary gland is damaged due to significant blood loss and hypovolemic shock (ischemic necrosis) usually during or after childbirth leading to decreased functioning of the pituitary gland (hypopituitarism). The pituitary gland is an endocrine organ, meaning it produces certain hormones and is involved in the regulation of various other hormones. This gland is located in the brain and sits in a pocket of the sphenoid bone known as the sella turcica. The pituitary gland works in conjunction with the hypothalamus, and other endocrine organs to modulate numerous bodily functions including growth, metabolism, menstruation, lactation, and even the "fight-or-flight" response. These endocrine organs release hormones in very specific pathways, known as hormonal axes. For example, the release of a hormone in the hypothalamus will target the pituitary to trigger the release of a subsequent hormone, and the pituitary's released hormone will target the next organ in the pathway. Hence, damage to the pituitary gland can have downstream effects on any of the aforementioned bodily functions. Signs and symptoms The various signs and symptoms in Sheehan's syndrome are caused by damage to the pituitary, thereby causing a decrease in one or more of the hormones it normally secretes. Since the pituitary controls many glands in the endocrine system, partial or complete loss of a variety of functions may result. Many of the signs and symptoms of Sheehan's are considered "nonspecific" in the medical community; in other words these signs and symptoms are seen in a number of different disease processes, and are not specific to a singular disease or syndrome. In some cases, a woman with Sheehan syndrome may be relatively asymptomatic initially; therefore, the diagnosis would not be made until years later when features of hypopituitarism become evident. In rare instances this syndrome can present acutely with unstable vital signs, dangerously low blood glucose levels, heart failure, or even psychosis. Hypopituitarism can lead to an interruption in any of the following hormone pathways: thyroid disorder (secondary hypothyroidism), adrenal gland (adrenal insufficiency due to glucocorticoid deficiency), sex hormone (gonadotropin deficiency), prolactin (a hormone responsible for lactation), growth hormone, or rarely anti-diuretic hormone deficiency (central diabetes insipidus). Since damage to the pituitary can cause a deficiency in more than one of these hormone pathways simultaneously, it is possible to have a mix of any of the signs or symptoms listed below. Sheehan's syndrome's most common initial symptoms are difficulties with or total absence of lactation (agalactorrhea). Another common sign is infrequent menstrual cycles (oligomenorrhea) or absent menstrual cycles (amenorrhea) following delivery. In addition to menstrual irregularities other signs of sex hormone deficiency are hot flashes, decreased libido, and breast involution. Symptoms and signs of thyroid disorder are tiredness, intolerance to cold, constipation, weight gain, hair loss, slowed thinking, as well as a slowed heart rate and low blood pressure. Adrenal gland malfunction can present acutely or chronically. In a more chronic case, it is similar to Addison's disease with symptoms including
Sheehan's syndrome