500px In both males and females,<unk>  works upon endocrine cells in the gonads to produce androgens. Effects in females<unk>  supports theca cells in the ovaries that provide androgens and<unk> l precursors for estradiol production. At the time of menstruation, FSH initiates follicular growth, specifically affecting granulosa cells. With the rise in estrogens,<unk>  receptors are also expressed on the maturing follicle, which causes it to produce more estradiol. Eventually, when the follicle has fully matured, a spike in 17α-hydroxyprogesterone production by the follicle inhibits the production of estrogens, leading to a decrease in estrogen-mediated negative feedback of GnRH in the hypothalamus, which then stimulates the release of<unk>  from the anterior pituitary. However another theory of the<unk>  peak is a positive feedback mechanism from estradiol. The levels keep rising through the follicular phase and when they reach an unknown threshold, this results in the peak of the<unk> . This effect is opposite from the usual negative feedback mechanism presented at lower levels. In other words, the mechanism(s) are not yet clear. The increase in<unk>  production only lasts for 24 to 48 hours. This "LH surge" triggers ovulation, thereby not only releasing the egg from the follicle, but also initiating the conversion of the residual follicle into a corpus luteum that, in turn, produces progesterone to prepare the endometrium for a possible implantation.<unk>  is necessary to maintain luteal function for the second two weeks of the menstrual cycle. If pregnancy occurs,<unk>  levels will decrease, and luteal function will instead be maintained by the action of hCG (human chorionic gonadotropin), a<unk>  very similar to<unk>  but secreted from the new placenta. Gonadal steroids (estrogens and androgens) generally have negative feedback effects on GnRH-1 release at the level of the hypothalamus and at the gonadotropes, reducing their sensitivity to GnRH. Positive feedback by estrogens also occurs in the gonadal axis of female mammals and is responsible for the midcycle surge of<unk>  that stimulates ovulation. Although estrogens inhibit kisspeptin (Kp) release from kiss1 neurons in the ARC, estrogens stimulate Kp release from the Kp neurons in the AVPV. As estrogens' levels gradually increase the positive effect predominates, leading to the<unk>  surge. GABA-secreting neurons that innervate GnRH-1 neurons also can stimulate GnRH-1 release. These GABA neurons also possess ERs and may be responsible for the GnRH-1 surge. Part of the inhibitory action of endorphins on GnRH-1 release is through inhibition of these GABA neurons. Rupture of the ovarian follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked increase in secretion of progesterone by the corpus luteum in the ovary, reinstating a predominantly negative feedback on hypothalamic secretion of GnRH-1. Effects in males<unk>  acts upon the Leydig cells of the testis and is regulated by gonadotropin-releasing<unk>  (GnRH). The Leydig cells produce testosterone under the control of<unk> .<unk>  binds to<unk>  receptors on the membrane surface of Leydig cells. Binding to this receptor causes an increase in cyclic adenosine monophosphate (cAMP), a secondary messenger, which allows cholesterol to translocate into the mitochondria. Within the mitochondria, cholesterol is converted to pregnenolone by CYP11A1. Pregnenolone is then converted to dehydroepiandrosterone (DHEA). DHEA is then converted to androstenedione by 3β-hydroxysteroid dehydrogenase (3β-HSD) and then finally converted to testosterone by 17β-hydroxysteroid dehydrogenase (HSD17B). The onset of puberty is controlled by two major<unk> s: FSH initiates spermatogenesis and<unk>  signals the release of testosterone, an androgen that exerts both endocrine activity and intratesticular activity on spermatogenesis.<unk>  is released from the pituitary gland, and is controlled by pulses of gonadotropin-releasing<unk> . When bloodstream testosterone levels are low, the pituitary gland is stimulated to release<unk> . As the levels of testosterone increase, it will act on the pituitary through a negative feedback loop and inhibit the release of GnRH and<unk>  consequently. Androgens (including testosterone and dihydrotestosterone) inhibit monoamine oxidase (MAO) in the pineal gland, leading to increased melatonin and reduced<unk>  and FSH by melatonin-induced increase of Gonadotropin-Inhibitory<unk>  (GnIH) synthesis and secretion. Testosterone can also be aromatized into estradiol (E2) to inhibit<unk> . E2 decreases pulse amplitude and responsiveness to GnRH from the hypothalamus onto the pituitary. Changes in<unk>  and testosterone blood levels and pulse secretions are induced by changes in sexual arousal in human males.
Luteinizing hormone
Menotropin
Antigonadotropin
Gonadotropin
Progonadotropin
Prolene
Testolactone
Allyltestosterone