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Background Yoga nidra is practised by sages for sleep. The practice is simple to use and has been clearly laid out, but its role in the treatment of chronic insomnia has not been well studied. Methods In this randomized parallel-design study conducted during 2012–16, we enrolled 41 patients with chronic insomnia to receive conventional intervention of cognitive behavioural therapy for insomnia (n=20) or yoga nidra (n=21). Outcome measures were both subjective using a sleep diary and objective using polysomnography (PSG). Salivary cortisol levels were also measured. PSG was done before the intervention in all patients and repeated only in those who volunteered for the same. Results Both interventions showed an improvement in subjective total sleep time (TST), sleep efficiency, wake after sleep onset, reduction in total wake duration and enhancement in subjective sleep quality. Objectively, both the interventions improved TST and total wake duration and increased N1% of TST. Yoga nidra showed marked improvement in N2% and N3% in TST. Salivary cortisol reduced statistically significantly after yoga nidra (p=0.041). Conclusion Improvement of N3 sleep, total wake duration and subjective sleep quality occurred following yoga nidra practice. Yoga nidra practice can be used for treatment of chronic insomnia after supervised practice sessions.

On 14th June 2021, Philips Respironics issued a medical device recall notification (US only) and field-safety notice (International Markets) for mechanical ventilator devices including continuous positive airway pressure (CPAP), and bilevel positive airway pressure (bilevel PAP). This was in response to potential health risks related to the sound abatement foam component in these devices. The company had stated that they are working hard towards a resolution, which includes repair and replacement of the affected devices. The statement of Philips clearly declares that this is a recall notification for the US, and only a field-safety notice for the rest of the world. The advisory from Philips puts the ball in the court of the physician or Durable Medical Equipment (DME) provider to determine the most appropriate options for continued treatment of patients using the affected devices. Although the long-term effects of these recalled machines will continue to be a matter of concern for the patients, the patients must be supported by the providers with explanations, reassurances and hope.

The modern life style demands a prolonged wakefulness despite the mounting evidences that deficit in adequate amount and quality of sleep impairs the wellbeing including attention, executive functions, working memory and other general functioning of the body. The thalamus plays a key role in mediating sleep–wakefulness through its intrinsic as well as extrinsic network connection with brainstem and cortex through ascending reticular activating system. In the present study, we examined the effects of 24, 48 and 72 h sleep deprivation in three separate groups of male Wistar rats on the thalamic grey matter volume. The three groups of rats (n = 18(6 × 3)) were sleep-deprived for three different durations, i.e. 24, 48 and 72 h using modified multiple platform method. Brain imaging was done using 7 T small animal MR scanner before and after sleep deprivation. From the acquired images, the total volume of the thalamus was calculated. The volume of the hippocampus was taken as reference. The grey matter volume of the thalamus showed a decreasing trend after sleep deprivation in all three groups of rats. Though the decrease in the thalamic volume was not statistically significant, the present study is the first animal MRI experiment to report the decrease in the thalamic grey matter volume after sleep deprivation which supports the similar findings in humans. The synaptic homeostatic hypothesis that cortical excitatory synapses should increase in size after wake and decrease after sleep is not evident in thalamus.

Orexinergic neurons in the lateral hypothalamic area project to the major wake-promoting areas of the brain and regulate many behavioural states. There are two subtypes of orexin neuropeptides (orexin-1, OX1, and orexin-2, OX2) that act on both orexin receptors 1 and 2 (OX1R and OX2R) in the brain. Some of the goal-oriented behaviour involves intense motor activities where orexin might be playing a role. During male sexual behaviour, the male rats indulge in intense motor activities while chasing the female to make sexual contact. In the present study, we utilized the male sexual behaviour model in rats to study the intense goal-oriented locomotor activity during motivated behaviour. The locomotor activity of sexually active male rats during sexual behaviour was assessed after 4 µl intracerebroventricular injection of either 50 nM of SB-334867 (OX1 receptor antagonist) or suvorexant (OX1 and OX2 receptor antagonist) in the presence of an estrous and a non-estrous female. Male rats treated with SB-334867 and suvorexant showed reduced locomotor activity during sexual behaviour in the presence of an estrous female. SB-334867 further delayed acts of male sexual behaviour by increasing pursuit latency, intromission latency, and mean inter-intromission interval. The overall sexual drive was also decreased in male rats treated with SB-334867. The results of this study suggest that orexin boosts goal-directed locomotor activities during sexually motivated behaviour.

Sleep is important for cognitive and physical performance. Sleep deprivation not only affects neural functions but also results in muscular fatigue. A good night’s sleep reverses these functional derangements caused by sleep deprivation. The role of sleep in brain function has been extensively studied. However, its role in neuromuscular junction or skeletal muscle morphology is sparsely addressed although skeletal muscle atonia and suspended thermoregulation during rapid eye movement sleep possibly provides a conducive environment for the muscle to rest and repair; somewhat similar to slow-wave sleep for synaptic downscaling. In the present study, we have investigated the effect of 24 h sleep deprivation on the neuromuscular junction morphology and neurochemistry using electron microscopy and immunohistochemistry in the rat soleus muscle. Acute sleep deprivation altered synaptic ultra-structure viz. mitochondria, synaptic vesicle, synaptic proteins, basal lamina, and junctional folds needed for neuromuscular transmission. Further acute sleep deprivation showed the depletion of the neurotransmitter acetylcholine and the overactivity of its degrading enzyme acetylcholine esterase at the neuromuscular junction. The impact of sleep deprivation on synaptic homeostasis in the brain has been extensively reported recently. The present evidence from our studies shows new information on the role of sleep on neuromuscular junction homeostasis and its functioning.Statement of significanceSleep causes synaptic downscaling in the brain, and allows the brain to carry out various housekeeping functions. Here we have reported that the function of the sleep-wake cycle on the synaptic homeostasis extends beyond the brain. Acute sleep deprivation caused significant alteration at ultra and macrostructure of antigravity muscle and the neuromuscular junction along with adaptation to new fiber type in rats. These morpho-functional changes were well correlated with the biochemical assessment of the acetylcholine at the neuromuscular junction. These changes were partially recovered when the rats were allowed to recover from sleep deprivation. The findings suggest a new avenue for a sleep study; employing the neuromuscular junction for exploring the effect of sleep at energy and synaptic homeostasis levels.

Background Sleep services are assigned a non-essential status during COVID-19. The American Academy of Sleep Medicine strongly urges sleep clinicians to continue postponing non-urgent care until a later date, if such a recommendation is made by state officials due to local conditions. At the same time, one cannot ignore the fact that sleep is important for people’s health and wellbeing. Therefore, to protect the health of the population, it is essential to find ways and means to continue the practice of sleep medicine even during the COVID-19 pandemic. Method Social environment and work ethics in sleep clinics and sleep laboratories in Asia, Africa, and Latin America are different from those in the US. Under these circumstances, the Indian Society for Sleep Research (ISSR) created a task force to develop guidelines for the practice of sleep medicine, not only for the Indian environment but also for other countries that are affected by the COVID-19 pandemic. The task force examined documents regarding practice of sleep medicine and associated specialities during COVID-19 by various professional organizations and governmental authorities. The recommendations were examined for their applicability. Wherever gaps were identified, consensus was reached keeping in view the available evidences. Outcome and Recommendations The emphasis of the guidelines is on avoiding doctor to patient contact during the pandemic. Teleconsultation and other modes of audio-visuals can be used as modes for medical practice during the COVID-19 pandemic. However, in addition to the patient, the presence of a family member, or a reliable informant is recommended. Patients of most sleep disorders can be provided tele-aftercare service. ISSR guidelines also give a list of medications allowed to be prescribed during the first and the follow-up teleconsultation. Hospitals and clinics are slowly opening in India and many other countries. As sleep services resume operations, there is a need to find innovative ways to reduce contact with COVID-19 patients, follow personal protection guidelines, as well as social distancing. This article does discuss strategies for the safe conduct of Level 1 sleep studies. Home sleep testing, which had greater acceptance during the last few years, should be given more attention during the COVID-19 period. Once the decision to reopen the sleep laboratory and resume operations is made, the safety of the patients and office staff should become the major priority. The ISSR recommendation is to postpone and reschedule in-laboratory positive pressure therapy, but it mentions the considerations to be followed in emergency situations. At the same time, high clinical risk patients may be diagnosed on the basis of clinical findings, and without performing polysomnography or home sleep testing. However, at some point, there is a need to reinitiate the in-lab testing. In addition, daily assessment of the COVID-19 situation in the community, along with a review of the situation with local public health and the state health department is advised.

Simultaneous and direct recording of temperature from the body, hypothalamus, and cortex in animals exposed to acute thermal challenges lack evidence. This study was conducted to assess the usual concept, that brain temperature is rather stable when animals are exposed to different ambient temperatures. In this study, we report the characteristic changes in the body, hypothalamic, and cortical temperature, when the rats were acutely exposed to cold (6 °C) and hot (36 °C) ambient temperature. The results of our study show that the body temperature is robustly regulated while hypothalamic and cortical temperatures vary on challenges to ambient cold (6 °C) and warm (36 °C) exposure in awake rats. The onset of response was observed quickest in the cortex, indicating that the cortical thermal sensing may relay intracranial thermal input to the hypothalamus for the regulation of body temperature within narrow limits. The present findings contradict earlier evidence, which stated that the brain does not participate in thermal sensing.

Available sleep deprivation studies lack data on simultaneous changes in hypothalamic, cortical and body temperature during sleep deprivation and recovery. Ten adult male Wistar rats chronically implanted with electroencephalogram, electro-oculogram and electromyogram electrodes for recording sleep were used in this study. Hypothalamic and cortical temperatures were measured by pre-implanted thermocouples. A radio transmitter (TA10TAF-40, DSI USA) was implanted intraperitoneally to measure body temperature. All the temperatures were measured simultaneously at 15-s intervals during baseline conditions, sleep deprivation and recovery sleep. Sleep deprivation was carried out for 24 hr by the gentle handling method; however, sleep and temperature were only recorded during the first 12 hr of deprivation. During sleep deprivation the body, hypothalamic and cortical temperatures increased significantly as compared to baseline. During recovery sleep, body and cortical temperature recovered earlier than the hypothalamic temperature. Hypothalamic temperature remained higher than the baseline values throughout 12 hr of recovery sleep. In the recovery sleep, cortical temperature decreased immediately and reached near baseline by 4 hr. We observed a quicker return of cortical temperature towards control temperature during recovery sleep compared with hypothalamic and body temperature. The results of the present study show that acute sleep deprivation results in a rise in both cortical and hypothalamic temperature, along with body temperature. A rise in cortical temperature may be a contributing factor for cognitive dysfunction resulting from sleep deprivation.

Transient receptor potential vanilloid 4 (TRPV4) ion channel is a non-selective cation channel and its role in cutaneous thermosensation is emerging. It is expressed in many areas of the brain including the preoptic area (POA)/anterior hypothalamus which is the key neural site for thermoregulation. The present study was conducted to find out the role of TRPV4 ion channel in the POA in thermoregulation. Rats preimplanted with guide cannulae with indwelling styli 2.0mm above the POA received TRPV4 agonist/antagonist/isotonic saline injections bilaterally in the POA using an injector cannula in three separate groups of six rats each. Body temperature (Tb) was recorded telemetrically by preimplanted radio transmitter in the peritoneal cavity. The injection of TRPV4 agonist (GSK1016790A) in the POA decreased Tb while its antagonist (RN1734) increased Tb. Immunohistochemical localization showed presence of TRPV4 ion channel in the POA. The results of the present study suggest that TRPV4 ion channels in the POA may play an important role in thermoregulation.

It has often been said that the brain is mostly benefitted from sleep. To understand the importance of sleep, extensive studies on other organs are too required. One such unexplored area is the understanding of muscle physiology during the sleep-wake cycle. Changes in muscle tone with different sleep phases are evident from the rapid eye movement sleep muscle atonia. There is variation in brain and body temperature during sleep stages, the brain temperature being higher during rapid eye movement sleep than slow-wave sleep. However, the change in muscle temperature with different sleep stages is not known. In this study, we have implanted pre-calibrated K-type thermocouples in the hypothalamus and the dorsal nuchal muscle, and a peritoneal transmitter to monitor the hypothalamic, muscle, and body temperature respectively in rats during 24 h sleep-wake cycle. The changes in muscle, body, and hypothalamic temperature during total sleep deprivation were also monitored. During normal sleep-wake stages, the temperature in the decreasing order was that of the hypothalamus, body, and muscle. Total sleep deprivation by gentle handling caused a significant increase in hypothalamic and body temperature, while there was least change in the muscle temperature. The circadian rhythm of the hypothalamic and body temperature in the sleep-deprived rats was disrupted, while the same was preserved in the muscle temperature. The results of our study show that muscle atonia during rapid eye movement sleep is a physiologically regulated thermally quiescent muscle state offering a conducive environment for muscle rest and repair.

Glutamate when microinjected at the medial preoptic area (mPOA) influences brain temperature (T br ) and body temperature (T b ) in rats. Glutamate and its various receptors are present at the mPOA. The aim of this study was to identify the contribution of each of the ionotropic glutamatergic receptors at the mPOA on changes in T br and T b in freely moving rats. Adult male Wistar rats (n=40) were implanted with bilateral guide cannula with indwelling styli above the mPOA. A telemetric transmitter was implanted at the peritoneum to record T b and locomotor activity (LMA). A precalibrated thermocouple wire implanted near the hypothalamus was used to assess T br . Specific agonist for each ionotropic glutamate receptor was microinjected into the mPOA and its effects on temperature and LMA were measured in the rats. The rats were also microinjected with the respective ionotropic receptor antagonists, 15 min prior to the microinjection of each agonist. Amongst amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl- d -aspartate (NMDA) and kainic acid, AMPA increased T b and LMA when injected at the mPOA. Specific antagonists for AMPA receptors was able to attenuate this increase (p br only. Microinjection of kainic acid and its antagonist had no effect on the variables. The finding of the study suggests that activation of the AMPA receptors at the mPOA, leads to the rise in body temperature.

India is an ancient country with a vast population, diverse geography and culture. Although sleep medicine has been rapidly progressing during the last decade in the country, the ancient Indian literature is rich in descriptions of sleep physiology and the importance of sleep in life. In spite of rapid industrialization and the emergence of a modern 24/7 h society, knowledge about sleep and its disorders is lacking amongst the general public and doctors. A need is felt to raise the level of awareness of sleep to that of the level of nutrition and exercise. There is shortage of trained certified sleep specialists and technicians to meet the emerging demand. A need is felt to provide standardized sleep health care service. The role of professional sleep societies, industry, private enterprises and government agencies in promoting sleep medicine education in the country is emphasized. Vertical integration of education in sleep physiology and disorders, from school level to graduate and postgraduate medical education, is advocated. To create specialists in the discipline, horizontal integration with physiology, neurology, psychiatry and pulmonary medicine is a viable solution in this multidisciplinary subject. The government should recognize sleep as an important public health issue.

Chronic insomnia is a common sleep problem and there is a need to complement the existing treatment options. Yoga nidra practice is documented to be used for sleep by sages. Recently, yoga nidra has been used in patients of menstrual abnormalities, post- traumatic stress disorder, diabetes, anxiety and depression but little is known about its effect on sleep or sleep disorders. Although we find description of yoga nidra in literature, there is no scientific report of its application in sleep disorders. The objective of the study was to develop yoga nidra model in management of chronic insomnia patients. The model was developed using inputs from yoga school trained instructors of yoga nidra. Patient 01: 60 years old widower with complaints of sleep maintenance insomnia since 20 years. He had worry at daytime regarding falling off to sleep which became even worse at bedtime. He had history of benign prostatic hypertrophy and had no history of any medications for sleep or any other disease. Patient 02: 78 years old male self-employed, company owner with complaints of sleep maintenance insomnia since 15 years. He felt quite energetic during the day due to the work requirement but in the evening started feeling anxious about sleep problem which worsened at bedtime. He was on tablet clonazepam 0.25 mg HS off and on since 1 year. After the baseline assessment, yoga nidra intervention was started followed by five supervised sessions after which the patients were instructed to practice yoga nidra daily on their own. Regular fortnightly follow ups were done till 4 weeks of start of yoga nidra intervention. Repeat PSG was offered in case patient volunteered. Sleep diary parameters were analysed using Friedman test and Wilcoxon Signed Ranks test. There was an improvement in sleep quality, insomnia severity, depression anxiety and stress scores after yoga nidra. The improvement remained even after 3 months of start of intervention. Repeat PSG in second patient showed an increase in N3 after 4 weeks of yoga nidra intervention. Yoga nidra can be used as an important adjunct in management of chronic insomnia patients. CTRI/2013/05/003682 [Registered on: 27/05/2013] Trial Registered Retrospectively.

The role of the preoptic area (POA) in thermoregulation is well documented. Microinjection of various neurotransmitters into the POA in rats has been shown to influence body temperature. Alhough there are reports showing changes in temperature on administration of L-glutamate into the POA, the role of this excitatory amino acid in thermoregulation has not been studied in unanaesthetized rats. In the present study, brain and body temperatures were recorded in freely moving adult male Wistar rats with K-type thermocouple implanted near the hypothalamus and temperature transmitter implanted inside the peritoneum. Recordings were performed 2 h preinjection and 4 h postinjection. L-glutamate (0.14 nM) microinjection into the POA induced long-lasting hyperthermia and reduced locomotor activity. The rats remained curled up and showed piloerection. L-glutamate-induced hyperthermia was attenuated by previous injection of the ionotropic L-glutamate receptor antagonist, kynurenate (0.11 nM). We propose that L-glutamate in the POA participates not only in heat production and conservation but also plays a role in interlinking sleep and thermoregulation.

Changes in ambient temperature produce complex effects on sleep–wakefulness. In order to find out the mechanisms involved in temperature-sensitive changes in sleep in rats, their thermal preference, body temperature and sleep were studied before and after the destruction of both peripheral and central warm receptors, by systemic administration of 375 mg/kg capsaicin. Though the pre-treated rats preferred to stay mostly at the ambient temperature of 27 °C, post-treated rats strayed freely into chambers having ambient temperature of 30 °C and 33 °C. Sleep and body temperature of these rats were studied for six hours each, when they were kept at an ambient temperature of 18–36 °C. Total sleep time, especially REM sleep, was maximum at 30 °C in pre-treated rats, but this REM sleep peak at 30 °C disappeared after capsaicin administration. Body temperature increased sharply in post-treated rats, at ambient temperatures above 30 °C. Apart from the ability to defend body temperature at high ambient temperature, avoidance of warm ambient temperature and increase in REM sleep are the behavioral measures which are lost in post-treated rats. Results of this study suggest that the ambient temperature-related increase in REM sleep at 30 °C could be part of the thermoregulatory measures.

The role of the medial septum in suppressing paradoxical sleep and promoting slow wave sleep was suggested on the basis of neurotoxic lesion studies. However, these conclusions need to be substantiated with further experiments, including chemical stimulation studies. In this report, the medial septum was stimulated in adult male rats by microinjection of L-glutamate. Sleep-wakefulness was electrophysiologically recorded, through chronically implanted electrodes, for 2 h before the injection and 4 h after the injection. There was a decrease in paradoxical sleep during the first hour and an increase in slow wave sleep during the second hour after the injection. The present findings not only supported the lesion studies but also showed that the major role of the medial septum is to suppress paradoxical sleep.

Changes in sleep and body temperature in rats at ambient temperatures below and above the self-selected temperature zone, are lacking in literature. In this report, the temperature preferred by the rats was first assessed before studying the changes in their sleep and body temperature, when they were exposed to ambient temperatures ranging from 18 degrees C to 36 degrees C. The rats preferred to stay at 27 degrees C when they were allowed to select their own ambient temperature, but maximum sleep was recorded when the rats were maintained at 30 degrees C. The ambient temperature-related changes in rapid eye movement sleep and deep slow wave sleep followed a bell-shaped curve, with a maximum at 30 degrees C. Of all the sleep parameters, rapid eye movement sleep showed a more marked ambient temperature-related change. Ambient temperatures above 33 degrees C and below 24 degrees C produced a significant reduction in sleep. Increase in sleep at 30 degrees C was associated with a slight elevation in body temperature, but a steep increase in body temperature at very high ambient temperature was associated with a decrease in sleep. Decrease in sleep at ambient temperatures below 24 degrees C was not related to any significant decrease in body temperature. Though maximum sleep was recorded at 30 degrees C, the sleep regulatory and thermoregulatory systems were at a functional equilibrium at 27 degrees C.

L -Glutamate is involved in the perception of umami taste, intermediary metabolism, and excitatory neurotransmission. In addition, recent studies have uncovered a variety of physiological roles for dietary glutamate, as evidenced by the fact that intragastric glutamate infusions induce flavor preference learning in rats. Moreover, glutamate increases digestive juice secretion and gastric emptying of protein-rich meals. Glutamate levels in blood and brain remain stable all day long even after the food intake since most of glutamate absorbed is oxidized in the mucosa of the small intestine as a primary energy source. Chronic ad libitum ingestion of glutamate solution contributes to reducing weight gain, fat deposition, and plasma leptin levels in comparison to ingestion of water. Glutamate receptors and their cellular transduction molecules have recently been identified in gut epithelial cells. Stimulation of gut glutamate receptors enhances the apical expression of glutamate transporters and also triggers the release of nitric oxide. Nitric oxide in its turn induces gut serotonin release, which increases vagal afferent inputs to different brain regions. Notably, three brain areas, i.e., the medial preoptic area, the dorsomedial nucleus of the hypothalamus, and the habenular nucleus are activated by intragastric glutamate infusions. Total subdiaphragmatic vagotomy abolishes this response. Consistent with the above, vagotomy specifically reduces the overall intake of glutamate. Taken together, these findings contribute to the growing body of evidence indicating that glutamate signaling via dedicated taste and gut receptors influences multiple physiological functions including gut secretion, motility, digestion, absorption, metabolism and energy homeostasis.

Several studies have shown the importance of the medial preoptic area in the regulation of sleep-wakefulness and of body temperature. The medial preoptic area has a rich noradrenergic innervation, coming mostly from the lateral tegmental noradrenergic system. The accumulating evidences show that the noradrenergic afferents to the medial preoptic area are involved in the induction of sleep. This hypnogenic mechanism operates through the postsynaptic alpha1 and alpha2-adrenergic receptors. Noradrenergic afferents are also involved in the thermoregulatory mechanisms, and the activation of these fibers brings about a fall in body temperature. Though the body temperature changes are brought about by the same receptor subtypes as those involved in hypnogenesis, observations suggest the possibility of separate sets of noradrenergic afferents in the medial preoptic area for sleep regulation and thermoregulation. In this review, we present the compelling evidences, which showed that the noradrenergic afferents of the medial preoptic area bring about a fall in body temperature and other thermoregulatory behavioral alterations associated with sleep.

Brain temperatures (Tbr) of male Wistar rats were recorded at every 15 min interval for 24 h, prior to the destruction of the medial septal (MS) neurons with N-methyl-D-aspartic acid, and on the 7th, 14th and 21st days after the destruction. The capacity of the rats to regulate their body temperature under severe cold and heat was assessed by recording their Tbr when they were exposed to 5+/-1 and 37+/-1 degrees C for 2 h, before lesion and on 8th, 9th, 15th, 16th, 22nd and 23rd days after the lesion. The Tbr was decreased and its circadian variation increased after the MS lesion. On exposure to an ambient temperature of 5+/-1 degrees C the Tbr was decreased on 9th and 16th days after the lesion, when compared with the sham lesion group on identical days, though the fall in temperature was not significant on the 23rd day. The change in Tbr (compared with the sham lesion group) was not significantly different on all days of exposure to 37+/-1 degrees C. The decrease in Tbr after the MS lesion is in contrast to the hyperthermia produced by lesion of the adjoining thermoregulatory areas. The present findings suggest that the MS lesions caused an alteration in the set point of body temperature, without drastic changes in thermoregulatory ability.

Earlier studies had indicated the possibility of the involvement of the alpha(1) adrenergic receptors on the medial preoptic (mPOA) neurons in hypnogenesis. Microinjection of alpha1 agonist methoxamine (0.05 microg) into the mPOA of the rats, maintained at an ambient temperature (Tamb) of 24 degrees C, did not produce any significant change in sleep-wakefulness (S-W), except for an arousal of short duration, which coincided with the steep fall in body temperature (Tb). It was probably not possible to elicit sleep, because of hypothermia simultaneously produced by this drug. To test this hypothesis, experiments were conducted in an environment where the effects of hypothermia could be partially compensated for. When the rats were allowed to select their Tamb, they moved over to a compartment having a higher Tamb of 30 degrees C, on administration of methoxamine into the mPOA. Simultaneously, there was induction of sleep, which lasted for 60 min. Thus, it was possible to demonstrate the hypnogenic action of methoxamine, which was masked by hypothermic action of the drug. The findings indicate that the alpha1 adrenergic receptors in the mPOA are involved in the induction of sleep.

Changes in sleep-wakefulness (S-W) were studied in adult male Wistar rats, along with body temperature (T(b)), locomotor activity (LMA) and thermal preference, after the lesion of the medial preoptic area (mPOA) with N-methyl-D-aspartic acid (NMDA). The sleep was decreased after the lesion of the mPOA, but there was recovery when the rats were given freedom to stay in an ambient temperature (T(amb)) which they preferred. When given a choice between three T(amb) (24, 27 and 30 degrees C), the rats preferred 27 degrees C before the mPOA lesion, and 24 degrees C during the initial days after the lesion. There was a shift in the thermal preference to 30 degrees C, on the fourth week after the lesion, which coincided with the considerable recovery of sleep. The preference for higher T(amb) probably helped to improve sleep, as T(amb) of 30 degrees C is known to promote sleep. When the lesioned rats were not given the freedom to select the T(amb), there was no recovery in sleep. The mPOA seems to be essential for increasing the durations of slow wave sleep (SWS) episodes, especially the light SWS (S1), as they remained shorter than the pre-lesion value, even when the rats were given freedom to stay in a preferred T(amb). The homeostatic recovery of sleep, especially the night time sleep, resulted in the disruption of circadian sleep rhythm. But, the LMA, T(b) and thermal preference maintained their diurnal variation. T(b) and LMA were elevated after the mPOA lesion and they remained so till the end of the study.

This study was aimed at correlating diurnal changes in thermal preference of rats with their body temperature (Tb), sleep-wakefulness (S-W) and locomotor activity (LMA). Electroencephalogram (EEG), electromyogram (EMG), electrooculogram (EOG) and Tb were recorded by telemetry, while an activity monitor measured LMA and thermal preference. A special environmental chamber, which was designed and fabricated, enabled for the first time, simultaneous measurement of thermal preference, along with S-W and Tb. S-W, thermal preference and LMA were recorded continuously in six adult male Wistar rats, for 24 h, for 3 days, and Tb with thermal preference and LMA were recorded for another 3 days. LMA and Tb were higher at night than during day. The rats slept less during the night time. Increased frequency of sleep episodes contributed towards increased sleep during day time. They preferred an ambient temperature (Tamb) of 24 degrees C at night and 27 degrees C during the day. Though the preference for higher Tamb during day time coincided with increased sleep, the rats did not move over to higher Tamb prior to the onset of sleep episodes. Though the diurnal alterations in sleep, Tb and LMA were similar to those reports from animals kept in constant Tamb, the day-night variation of paradoxical sleep (PS) was exaggerated when the rats selected their own preferred Tamb.

The study was aimed at investigating the possible involvement of noradrenergic mechanisms in the lateral septum (LS) for elaboration of male sexual behavior in rats. In this study, norepinephrine (NE), yohimbine (YOH), isoproterenol (ISOP), propranolol (PROP), saline (SAL) and dimethyl sulfoxide (DMSO) were injected bilaterally in the LS in six different groups of sexually active male rats, and various components of sex behavior were recorded. The application of NE (3 microg) and alpha(2)-antagonist YOH (1 microg) produced a stimulation of most of the components of male sexual behavior, and there was increase in sexual arousal as well as performance. The microinfusion of nonspecific beta-agonist ISOP (2 microg) also produced a stimulation of copulatory behavior whereas beta-antagonist PROP (2 microg) produced an inhibition. The stimulation of male sexual behavior by YOH application at the LS could be due to an increased release of NE by its blocking effect on presynaptic alpha(2)-receptors. These results suggest that the noradrenergic system in the LS has stimulatory effect upon male sexual behavior, probably acting through beta-receptors.

Monosodium glutamate, a umami taste substance is commonly used flavor enhancer. The effect of intragastric administration of 1.5 ml of 0.12 M monosodium glutamate on sleep–wake was studied in 10 adult male Wistar rats. Sleep–wake parameters were recorded through chronically implanted electroencephalogram, electrooculogram and electromyogram electrodes using a digital recording system (BIOPAC system Inc. BSL PRO 36, USA). The sleep–wake was recorded for 6 h after the intragastric administration of either glutamate or saline. Sleep–wake stages were analyzed as wake, slow wave sleep and REM sleep. Compared to saline, intragastric administration of glutamate significantly increased REM sleep duration and episode frequency. REM sleep duration was increased in all the three 2 h bins, 10:00–12:00 h (p = 0.037), 12:00–14:00 h (p = 0.037) and 14:00–16:00 h (p = 0.007). The slow wave sleep and total sleep time were not affected. It is concluded that intragastric glutamate administration increases REM sleep.

Exposure to cold ambient temperature (Ta) affects sleep-wake (S-W) state. The vigilance states on the other hand influence thermal status of the animals. Simultaneous recording of body temperature (Tb) with S-W is crucial to understand the homeostatic relationship between the two. In the present study we recorded both Tb and hypothalamic temperature (Thy) along with S-W, during acute and chronic exposure to mild cold (Ta). Electrooculogram (EOG), electroencephalogram (EEG) and electromyogram (EMG) electrodes were chronically implanted in rats to assess S-W. A thermocouple, near the preoptic area, and radio transmitter in the peritoneum, were implanted, to record Thy and Tb respectively. After three days of baseline recordings of S-W, Thy and Tb at Ta of 26 dergrees C, the rats were exposed to mild cold Ta (18 degrees C) for 28 days. All the parameters were recorded during cold exposure and also for five days after the termination of cold exposure. On the first day of cold exposure there was a decrease in slow wave sleep and paradoxical sleep, but they were restored by the 21st day of continued exposure. The Thy remained decreased throughout the cold exposure. Though the Tb showed a slight decrease on the first day of cold exposure, there was no appreciable change during the subsequent days. The Thy came back to near pre exposure level on termination of cod exposure. The decrease in Thy during mild cold exposure would have triggered cold defense mechanisms. Increase in wakefulness during acute cold exposure and non-shivering thermogenesis during chronic cold exposure are probably responsible for the maintenance of Tb. Decrease in Thy is probably the key trigger for initiating thermoregulatory measures to maintain Tb and homeostatic restoration of sleep.

Orexins are important regulators of sleep-wakefulness (S-W). Rats were intracerebroventricularly (ICV) administered selective orexin-2 receptor antagonist, TCS-OX2-29. There was decreased wakefulness due to a decrease in the average wake episode duration and an increased REM sleep due to an increase in the number of REM episodes, indicating an inhibitory role of the central orexin-2 receptors on REM sleep generation.

Warm sensitive neurons (WSN) play a major role not only in body temperature regulation, but also in sleep regulation. The present study was undertaken to investigate the role of WSN of the preoptic area (POA) in mediating the ambient temperature (T(amb)) related changes in sleep. The effect of T(amb) changes on sleep and body temperature was studied in rats before and after destruction of WSN of the POA by local intracerebral injection of capsaicin. Though the rats preferred 27 degrees C T(amb), they slept maximum at 30 degrees C. After destruction of WSN of the POA, slow wave sleep (SWS) peak was brought down to 27 degrees C, which was the preferred T(amb) of the rats. This indicates that WSN of the POA mediate the increase in SWS, at temperatures higher than preferred T(amb). On the other hand, in WSN destroyed rats, rapid eye movement (REM) sleep was maximum at 33 degrees C. It suggests that the REM sleep generation is under inhibitory control of the WSN of the POA. The study supports several earlier reports that the neurons of the POA play a key role in coordinating sleep and body temperature regulation.

Regulation of body temperature and sleep are two physiological mechanisms that are vital for our survival. Interestingly neural structures implicated in both these functions are common. These areas include the medial preoptic area, the lateral preoptic area, the ventrolateral preoptic area, the median preoptic nucleus and the medial septum, which form part of the basal forebrain. When given a choice, rats prefer to stay at an ambient temperature of 270C, though the maximum sleep was observed when they were placed at 300C. Ambient temperature around 270C should be considered as the thermoneutral temperature for rats in all sleep studies. At this temperature the diurnal oscillations of sleep and body temperature are properly expressed. The warm sensitive neurons of the preoptic area mediate the increase in sleep at 300C. Promotion of sleep during the rise in ambient temperature from 270C to 300C, serve a thermoregulatory function. Autonomous thermoregulatory changes in core body temperature and skin temperature could act as an input signal to modulate neuronal activity in sleep-promoting brain areas. The studies presented here show that the neurons of the basal forebrain play a key role in regulating sleep. Basal forebrain thermoregulatory system is a part of the global homeostatic sleep regulatory mechanism, which is auto-regulated.

The finding that glycine potentiates N-methyl-D-aspartate (NMDA) receptor-mediated responses, has tremendously changed our understanding of glutamatergic synaptic transmission in the brain. Although the phenomenon has been confirmed in number of preparations, it is yet to be demonstrated in awake animals. Further, the controversy that glycine binding sites of NMDA receptor are saturated in vivo or not, can be best verified in awake animals. Here, we have demonstrated that glycine enhanced glutamate-induced neuronal discharges in the ventromedial nucleus of the hypothalamus of awake behaving rats using microiontophoresis technique, suggesting that the glycine binding sites of NMDA receptor are not saturated under physiological conditions.

A large body of evidence has established the role of the medial preoptic area (mPOA) in regulation of slow wave sleep (SWS). Although the mPOA neurons contain excitatory neurotransmitter glutamate, its role in sleep–wakefulness is not known. In the present study microinjection of monosodium glutamate (40, 80 and 120 ng) into the mPOA augmented SWS. Earlier reports have shown enhancement of paradoxical sleep by glutamate in other brain areas.

The available information on simultaneous assessment of body and hypothalamic temperatures in rats are lacking. In the present study these temperatures were recorded for 24 h, on three alternate days, in rats maintained at an ambient temperature of 26 +/- 1 degrees C. Hypothalamic temperature was significantly higher than body temperature during the night. In nocturnal rats the magnitude of circadian variation in hypothalamic temperature was higher than body temperature. Though maintained at different levels, both the temperatures showed closely associated diurnal changes throughout the 24 h period.

l-Glutamate is a multifunctional amino acid involved in taste perception, intermediary metabolism, and excitatory neurotransmission. In addition, recent studies have uncovered new roles for l-glutamate in gut-brain axis activation and energy homeostasis. l-Glutamate receptors and their cellular transduction molecules have recently been identified in gut epithelial cells. Stimulation of such l-glutamate receptors by luminal l-glutamate activates vagal afferent nerve fibers and then parts of the brain that are targeted directly or indirectly by these vagal inputs. Notably, 3 areas of the brain-the medial preoptic area, the hypothalamic dorsomedial nucleus, and the habenular nucleus-are activated by intragastric l-glutamate but not by glucose or sodium chloride. Furthermore, the chronic, ad libitum ingestion of a palatable solution of monosodium l-glutamate (1% wt:vol) by rats has also been found to reduce weight gain, fat deposition, and plasma leptin concentrations compared with rats that ingest water alone. No difference in food intake was observed. Such effects may also be vagally mediated. Together, such findings contribute to the growing knowledge base that indicates that l-glutamate signaling via taste and gut l-glutamate receptors may influence multiple physiologic functions, such as thermoregulation and energy homeostasis.

The chronic changes in sleep-wakefulness (S-W), body temperature (Tb), locomotor activity (LMA) and thermal preference were studied in male Wistar rats after the destruction of neurons in both the medial preoptic area (mPOA) and the medial septum (MS) by intracerebral injection of N-methyl-D-aspartic acid. An increase in the Tb, and a preference for higher ambient temperature (Tamb) of 30 degrees C were observed after the combined lesion of the mPOA and the MS. Similar changes were reported to occur after the lesion that was restricted to the mPOA. But these alterations were in contrast to the decrease in Tb and preference for lower Tamb, observed after the MS lesion. The thermostat of the brain would have been reset at a higher level after the combined lesion, as there was an increase in Tb, along with a preference for a higher Tamb, and an increase in LMA. There was a reduction in the frequency and the duration of the slow wave sleep (SWS) episodes, and a reduction in the frequency of the paradoxical sleep (PS) episodes after the combined lesion. The destruction of the MS neurons was probably responsible for the reduction in the frequency of SWS, whereas the loss of mPOA neurons was responsible for the decrease in the duration of SWS and frequency of PS. It can be suggested that the MS exerts its influence on thermoregulation through the mPOA. However, the MS and the mPOA seem to play independent, but complementary roles in sleep promotion.

Afferents from the perirhinal cortex (PRh) form a major input to the hippocampal formation, which is known to be involved in sexual behavior in rodents. But there is a lacuna in literature regarding the role of the PRh in sexual behavior. Bilateral neurotoxic lesions of the PRh delayed the ejaculation latency and prolonged the mean inter-intromission interval significantly, suggesting a facilitatory role of the PRh in male rat sex behavior.

This paper reviews the recent studies that led to the conclusion that the noradrenergic neurons projecting to the medial preoptic area (mPOA) are hypnogenic and that they mediate this action through alpha(1) adrenergic receptors. Microinjection of noradrenaline (NA) into the mPOA induced arousal. Studies using alpha(2) adrenergic drugs showed that the arousal induced by intrapreoptic injection of NA was due to its action on presynaptic alpha(2) adrenergic receptors. A combination of lesion and chemical stimulation techniques demonstrated that when NA acted on the postsynaptic alpha(1 )receptors in the mPOA, it induced sleep. Intrapreoptic injection of alpha(1) agonist, methoxamine could induce sleep, when the hypothermia, which was simultaneously produced, was behaviorally compensated for by the animal. Increased arousal produced by the destruction of noradrenergic fibers in the mPOA further confirmed the hypnogenic role of these fibers.

The effects of chronic exposure to a mildly cold ambient temperature (T(a)) of 18 degrees C on sleep wakefulness (S-W) and brain temperature (T(br)) were studied in the medial preoptic area (mPOA) lesioned male Wistar rats. Electroencephalogram (EEG), electrooculogram (EOG) and electromyogram (EMG) electrodes were chronically implanted to assess S-W, and a thermocouple above the dura to record the T(br). After three recordings (24 h each) of S-W and T(br) at 24 degrees C, N-methyl D-aspartic acid (NMDA) was intracerebrally injected to produce bilateral destruction of neurons in the mPOA. There was decreased sleep and increased T(br) even four weeks after the mPOA lesion. T(a) of the environmental chamber was then reduced to 18 degrees C, and the S-W and T(br) were again recorded for 24 h each on the 1st, 7th, 14th, 21st, and on 28th days of continuous exposure to the mild cold T(a). Exposure to the cold produced further decrease in sleep and increase in the T(br). However, sleep came back to the pre-exposure level by the 14th day. An increase in the duration of sleep episodes was responsible for the restoration of sleep during chronic cold exposure. The study showed that the requirement of sleep was reset at a lower level in the mPOA lesioned rats. The mPOA lesion affected the sleep maintenance and sleep initiation, though the latter became evident only during chronic cold exposure. The magnitude of the acute changes in T(br) and S-W were less in the lesioned rats, as compared to those observed in the normal rats exposed to similar cold T(a). On the basis of these observations, it could be proposed that the mPOA plays some role in cold induced changes in thermoregulation and sleep regulation. The T(br) remained elevated throughout the period of cold exposure. Resetting of the T(br), at a higher level may be part of the homeostatic readjustment to restore sleep.