Electrical activity in the brain Polysomnographic record of<unk> . EEG highlighted by red box.<unk><unk>  highlighted by red line.<unk>  is coined "paradoxical" because of its similarities to wakefulness. Although the body is paralyzed, the brain acts as if it is somewhat awake, with cerebral neurons firing with the same overall intensity as in wakefulness. Electroencephalography during<unk>  deep sleep reveals fast, low amplitude, desynchronized neural oscillation (brainwaves) that resemble the pattern seen during wakefulness, which differ from the slow δ (delta) waves pattern of NREM deep sleep. An important element of this contrast is the 3–10 Hz theta rhythm in the hippocampus and 40–60 Hz gamma waves in the cortex; patterns of EEG activity similar to these rhythms are also observed during wakefulness. The cortical and thalamic neurons in the waking and<unk> ing brain are more depolarized (fire more readily) than in the NREM deep sleeping brain. Human theta wave activity predominates during<unk>  in both the hippocampus and the cortex. During<unk> , electrical connectivity among different parts of the brain manifests differently than during wakefulness. Frontal and posterior areas are less coherent in most frequencies, a fact which has been cited in relation to the chaotic experience of dreaming. However, the posterior areas are more coherent with each other; as are the right and left hemispheres of the brain, especially during lucid dreams. Brain energy use in<unk> , as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower. Brain stem Neural activity during<unk>  seems to originate in the brain stem, especially the pontine tegmentum and locus coeruleus.<unk>  is punctuated and immediately preceded by PGO (ponto-geniculo-occipital) waves, bursts of electrical activity originating in the brain stem. (PGO waves have long been measured directly in cats but not in humans because of constraints on experimentation; however, comparable effects have been observed in humans during "phasic" events which occur during<unk> , and the existence of similar PGO waves is thus inferred.) These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep. They exhibit their highest amplitude upon moving into the visual cortex and are a cause of the "rapid<unk><unk> s" in paradoxical sleep. Other muscles may also contract under the influence of these waves. Forebrain Research in the 1990s using positron emission tomography (PET) confirmed the role of the brain stem and suggested that, within the forebrain, the limbic and paralimbic systems showed more activation than other areas. The areas activated during<unk>  are approximately inverse to those activated during non-REM sleep and display greater activity than in quiet waking. The "anterior paralimbic<unk>  activation area" (APRA) includes areas linked with emotion, memory, fear and sex, and may thus relate to the experience of dreaming during<unk> . More recent PET research has indicated that the distribution of brain activity during<unk>  varies in correspondence with the type of activity seen in the prior period of wakefulness. The superior frontal gyrus, medial frontal areas, intraparietal sulcus, and superior parietal cortex, areas involved in sophisticated mental activity, show equal activity in<unk>  as in wakefulness. The amygdala is also active during<unk>  and may participate in generating the PGO waves, and experimental suppression of the amygdala results in less<unk> . The amygdala may also regulate cardiac function in lieu of the less active insular cortex. Chemicals in the brain Compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves. The monoamine neurotransmitters norepinephrine, serotonin and histamine are completely unavailable. Injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. Carbachol, which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monoamine neurotransmitters have already been depleted. Two other neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep. Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation. Models of<unk>  regulation According to the activation-synthesis hypothesis proposed by Robert McCarley and Allan Hobson in 1975–1977, control over<unk>  involves pathways of "REM-on" and "REM-off" neurons in the brain stem.<unk> -on neurons are primarily cholinergic (i.e., involve acetylcholine);<unk> -off neurons activate serotonin and noradrenaline, which among other functions suppress the<unk> -on neurons. McCarley and Hobson suggested that the<unk> -on neurons actually stimulate<unk> -off neurons, thereby serving as the mechanism for the cycling between<unk>  and non-REM sleep. They used Lotka–Volterra equations to describe this cyclical inverse relationship. Kayuza Sakai and Michel Jouvet advanced a similar model in 1981. Whereas acetylcholine manifests in the cortex equally during wakefulness and<unk> , it appears in higher concentrations in the brain stem during<unk> . The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters; researchers in recent years increasingly include GABA regulation in their models.<unk><unk> s Most of the<unk><unk> s in "rapid<unk><unk> " sleep are in fact less rapid than those normally exhibited by waking humans. They are also shorter in duration and more likely to loop back to their starting point. About seven such loops take place over one minute of<unk> . In slow-wave sleep, the<unk> s can drift apart; however, the<unk> s of the paradoxical sleeper move in tandem. These<unk><unk> s follow the ponto-geniculo-occipital waves originating in the brain stem. The<unk><unk> s themselves may relate to the sense of vision experienced in the dream, but a direct relationship<unk> ains to be clearly established. Congenitally blind people, who do not typically have visual imagery in their dreams, still move their<unk> s in<unk> . An alternative explanation suggests that the functional purpose of<unk>  is for procedural memory processing, and the rapid<unk><unk>  is only a side effect of the brain processing the<unk> -related procedural memory. Circulation, respiration, and thermoregulation Generally speaking, the body suspends homeostasis during paradoxical sleep. Heart rate, cardiac pressure, cardiac output, arterial pressure, and breathing rate quickly become irregular when the body moves into<unk> . In general, respiratory reflexes such as response to hypoxia diminish. Overall, the brain exerts less control over breathing; electrical stimulation of respiration-linked brain areas does not influence the lungs, as it does during non-REM sleep and in waking. The fluctuations of heart rate and arterial pressure tend to coincide with PGO waves and rapid<unk><unk> s, twitches, or sudden changes in breathing. Erections of the penis (nocturnal penile tumescence or NPT) normally accompany<unk>  in rats and humans. If a male has erectile dysfunction (ED) while awake, but has NPT episodes during<unk> , it would suggest that the ED is from a psychological rather than a physiological cause. In females, erection of the clitoris (nocturnal clitoral tumescence or NCT) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). During a normal night of sleep, the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during<unk> . Body temperature is not well regulated during<unk> , and thus organisms become more sensitive to temperatures outside their thermoneutral zone. Cats and other small furry mammals will shiver and breathe faster to regulate temperature during NREMS—but not during<unk> . With the loss of muscle tone, animals lose the ability to regulate temperature through body<unk> . (However, even cats with pontine lesions preventing muscle atonia during<unk>  did not regulate their temperature by shivering.) Neurons which typically activate in response to cold temperatures—triggers for neural thermoregulation—simply do not fire during<unk> , as they do in<unk>  and waking. Consequently, hot or cold environmental temperatures can reduce the proportion of<unk> , as well as amount of total sleep. In other words, if at the end of a phase of deep sleep, the organism's thermal indicators fall outside of a certain range, it will not enter paradoxical sleep lest deregulation allow temperature to drift further from the desirable value. This mechanism can be 'fooled' by artificially warming the brain. Muscle<unk>  atonia, an almost complete paralysis of the body, is accomplished through the inhibition of motor neurons. When the body shifts into<unk> , motor neurons throughout the body undergo a process called hyperpolarization: their already-negative membrane potential decreases by another 2–10 millivolts, thereby raising the threshold which a stimulus must overcome to excite them. Muscle inhibition may result from unavailability of monoamine neurotransmitters (restraining the abundance of acetylcholine in the brainstem) and perhaps from mechanisms used in waking muscle inhibition. The medulla oblongata, located between pons and spine, seems to have the capacity for organism-wide muscle inhibition. Some localized twitching and reflexes can still occur. Pupils contract. Lack of<unk>  atonia
Rapid eye movement sleep
Twilight sleep
Sleep onset
Free-running sleep
Non-rapid eye movement sleep
Slow-wave sleep
Postictal state
Nightmare