A sleep inducing factor from common Indian toad (Bufo melanostictus, Schneider) skin extract (original) (raw)
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Some Experiments in the Chemistry of Normal Sleep
British Journal of Psychiatry, 1966
Sleep is essential for physical and mental health. In the last 15 years there has grown up the concept of the brain stem reticular activating system. Electroencephalographic studies have shown two qualitatively different and alternating kinds of sleep, the orthodox (“slow wave”, or “forebrain“) and the paradoxical (”hind-brain“, “rapid eye movement”, “activated“, or “dreaming”) phases (Akertet al., 1965). It may be predicted that in the next decade attention will turn increasingly to the chemical basis of sleep. If a man is deprived of sleep for 100 hours, it is extremely difficult to keep him awake and one may suppose that an abnormal biochemical state exists within his central nervous system.
Modification of REM sleep and associated phasic activities by protein synthesis inhibitors
Experimental Neurology, 1979
The sleep-wake cycle and multiple-unit activity following the administration of various doses of protein synthesis inhibitors was studied in unrestrained cats. Special care was taken to analyze the effects of those drugs on phasic and tonic rapid eye movement (REM) sleep periods. It was observed that protein synthesis inhibitors decreased specifically total REM sleep time, at the expense of wakefulness, without altering slow-wave sleep time. It was further noted that the reduction in REM sleep was the result of a decrease in the frequency of REM periods, rather than in the duration of each individual period. In addition, protein synthesis inhibitors decreased phasic REM sleep and notably prolonged tonic REM periods. Moreover the phasic bursts of multiple-unit activity normally seen during REM sleep in control recordings were practically absent during REM sleep after the administration of protein synthesis inhibitors. It is suggested that protein molecules may participate in the mechanisms which trigger REM sleep.
The role of mesopontine NGF in sleep and wakefulness
Brain Research, 2011
The microinjection of nerve growth factor (NGF) into the cat pontine tegmentum rapidly induces rapid eye movement (REM) sleep. To determine if NGF is involved in naturally-occurring REM sleep, we examined whether it is present in mesopontine cholinergic structures that promote the initiation of REM sleep, and whether the blockade of NGF production in these structures suppresses REM sleep. We found that cholinergic neurons in the cat dorsolateral mesopontine tegmentum exhibited NGF-like immunoreactivity. In addition, the microinjection of an oligodeoxyribonucleotide (OD) directed against cat NGF mRNA into this region resulted in a reduction in the time spent in REM sleep in conjunction with an increase in the time spent in wakefulness. Sleep and wakefulness returned to baseline conditions 2 to 5 days after antisense OD administration. The preceding antisense OD-induced effects occurred in conjunction with the suppression of NGF-like immunoreactivity within the site of antisense OD injection. These data support the hypothesis that NGF is involved in the modulation of naturally-occurring sleep and wakefulness.
Clues to the functions of mammalian sleep
Nature, 2005
The functions of mammalian sleep remain unclear. Most theories suggest a role for non-rapid eye movement (NREM) sleep in energy conservation and in nervous system recuperation. Theories of REM sleep have suggested a role for this state in periodic brain activation during sleep, in localized recuperative processes and in emotional regulation. Across mammals, the amount and nature of sleep are correlated with age, body size and ecological variables, such as whether the animals live in a terrestrial or an aquatic environment, their diet and the safety of their sleeping site. Sleep may be an efficient time for the completion of a number of functions, but variations in sleep expression indicate that these functions may differ across species. Saying that it is desirable to be well rested and that the body seeks lost sleep with a vigour comparable to or greater than that displayed for food or sex does not answer the question of the functional role of sleep. Why do we spend one-third of our lives asleep? Why has our body evolved to press us relentlessly to make up for lost sleep? Can we separate the drive for sleep, manifested in sleepiness, from the function of sleep, as we can separate hunger from the benefits of food consumption? Why do so many species habitually sleep much more than humans, and others much less, and how do species that sleep for only short periods accomplish the functions of sleep in less time? Why does the daily sleep amount decrease from birth to maturity in all species of terrestrial mammals? And why do we have two kinds of sleep, rapid eye movement (REM) and non-REM (NREM) sleep? Sleep can be defined as a state of immobility with greatly reduced responsiveness, which can be distinguished from coma or anaesthesia by its rapid reversibility. An additional defining characteristic of sleep is that when it is prevented, the body tries to recover the lost amount. The existence of sleep 'rebound' after deprivation 1 demonstrates that sleep is not simply a period of reduced activity or alertness regulated by circadian or ultradian rhythms, a phenomenon that can be seen even in non-sleeping organisms 2-4. The amplitude of the changes in brain metabolism and neuronal activity that occurs during sleep exceeds those which occur during most waking periods 5-7. The argument that sleep serves a vital function is compelling. Sleep deprivation in rodents and flies can cause death more quickly than food deprivation 8. Nevertheless, we must not assume that the effects of sleep loss are independent of the deprivation technique used or that sleep loss has equally dire effects in all animals 9,10. In this review we will consider the vast knowledge that has been gained about the physiological nature of sleep and sleep-control mechanisms, evidence from sleep-deprivation studies and the distribution of sleep across species in the context of theories of sleep function. These data support theories that suggest that sleep saves energy, keeps species from being active at inopportune times and reverses wakinginduced changes in brain function. The evidence suggests distinct roles for REM and NREM sleep. It is also clear that sleep expression is adapted to ecological factors and may differ qualitatively across species. Sleep-controlling brain regions in mammals Neurophysiological studies have provided considerable information about the mechanisms controlling sleep states. These data can guide theories of sleep functions. Detailed reviews of the physiological control of sleep are available elsewhere 11 , but for the purposes of the current review, several aspects will be highlighted. NREM sleep phenomena can be generated by the isolated forebrain 12-14. Groups of sleep-active neurons have been discovered in the preoptic and basal forebrain regions (Fig. 1). These cells are maximally active during NREM sleep, and when stimulated will induce this state. Conversely, damage to these regions greatly reduces sleep. These neurons act through direct and indirect inhibitory projections to aminergic, cholinergic and hypocretinergic (also called orexinergic) neurons in the forebrain and brainstem. These and other neuronal groups maintain waking. The preoptic and anterior hypothalamic regions, within which most of these sleep-active neurons are embedded, have central roles in controlling the body and brain's temperature 15. Many sleep-active neurons are thermosensitive; when studied in tissue slices and in the intact brain they increase their activity at higher temperatures 12. Heating of the preoptic regions increases NREM sleep. REM sleep phenomena can be generated by the isolated brainstem,
The effects of various protein synthesis inhibitors on the sleep-wake cycle of rats
Psychopharmacology, 1977
The present investigation sought to determine the effects of Anisomycin (A), Chloramphenicol (ChA), Vincristine (V), and Penicilline G on the sleep-wake cycle of rats. It was found that both high and low doses of anisomycin decreased rapid eye movement (REM) sleep, while only high doses of ChA and V produced such a decrease. Slow wave sleep (SWS) was unaffected by these drugs. Penicilline G, on the other hand, had no effect on the sleep-wake cycle. It was further shown that the reduction of REM sleep was the result of a decrease in the number of REM periods rather than in the duration of each individual period. These results suggest that protein synthesis may participate in the mechanisms that trigger REM sleep.
Sleep Medicine Clinics
Behavioral states alternate between wakefulness and sleep, which is further subdivided into rapid-eye-movement sleep and non-rapid-eye-movement sleep. Waking and sleep states are highly complex processes that are elegantly orchestrated by fine-tuned neurochemical changes, including the neurotransmitters and neuromodulators glutamate, acetylcholine,-amino-butyric acid, norepinephrine, dopamine, serotonin, histamine, hypocretin, melanin concentrating hormone, adenosine, and melatonin. However, as highlighted in this brief overview, no single neurotransmitter or neuromodulator, but rather their complex interactions within organized neuronal ensembles, regulate waking and sleep states and drive their transitions. Dysregulation of and medications interfering with these neurochemical systems lead to sleep-wake disorders and functional changes of wakefulness and sleep. The neurochemical pathways presented here, thus, are aimed to provide a conceptual framework for the understanding of the effects of currently used medications on wakefulness and sleep.
Updates Regarding Neurocircuits and Neurotransmitters Involved in the Regulation of Wakefulness
Sohag Medical Journal
Sleep is a universal phenomenon that is observed not only in humans but also in birds, fishes, and flies even in simpler organisms such as worms also we spend about 8 hours each day in sleep which represents nearly one-third of our life. All these observations indicate the physiological importance of sleep. study of sleep mechanisms requires the first study of the mechanisms, neurocircuits, and neurotransmitters involved in the promotion of wakefulness. Observation of Von Economo in 1930 of patients affected by "encephalitis lethargica", an epidemic that causes widespread and prolonged sleepiness most of the day, opened the door for the study of the brain regions responsible for wakefulness. Researchers recognized now many brain regions that are responsible for wakefulness and other brain regions responsible for the induction of different types of sleep. This review will try to discuss the most recent mechanisms and neural circuits involved in the promotion of wakefulness.