Cold exposure and sleep in the rat: REM sleep homeostasis and body size.

Study Objectives: Exposure to low ambient temperature (Ta) depresses REM sleep (REMS) occurrence. In this study, both short and long-term homeostatic aspects of REMS regulation were analyzed during cold exposure and during subsequent recovery at Ta 24 degrees C.

Design: EEG activity, hypothalamic temperature, and motor activity were studied during a 24-h exposure to Tas ranging from 10 degrees C to -10 degrees C and for 4 days during recovery.

Carotid blood flow during REM sleep.

Objective: The present study was aimed at directly appraising, in the rabbit, the decrease in common carotid blood flow, the occurrence of which during REM sleep was indirectly suggested by previous studies of preoptic-hypothalamic temperature changes during sleep.

Methods: In 5 unrestrained male rabbits, polygraphic recordings of electroencephalography, electromyography, ear pinna temperature (degree C), common carotid mean and peak blood flow (mL/min), and heart rate (beats/min) were carried out across ultradian wake-sleep cycles. In each cycle, epochs of 60 seconds were selected for analysis at the end of non-rapid eye movement (NREM) sleep, at the beginning and end of rapid eye movement (REM) sleep, and at the beginning of the subsequent period of wakefulness.

Cold exposure and sleep in the rat: effects on sleep architecture and the electroencephalogram.

Study Objectives: Acute exposure to low ambient temperature modifies the wake-sleep cycle due to stage-dependent changes in the capacity to regulate body temperature. This study was carried out to make a systematic analysis of sleep parameters during the exposure to different low ambient temperatures and during the following recoveries at ambient temperature 24 degrees C.

Design: Electroencephalographic activity, hypothalamic temperature, and motor activity were studied during a 24-hour exposure to ambient temperatures ranging from 10 degrees C to -10 degrees C and for 4 days during the recovery.

Changes in EEG activity and hypothalamic temperature as indices for non-REM sleep to REM sleep transitions.

A shift of physiological regulations from a homeostatic to a non-homeostatic modality characterizes the passage from non-NREM sleep (NREMS) to REM sleep (REMS). In the rat, an EEG index which allows the automatic scoring of transitions from NREMS to REMS has been proposed: the NREMS to REMS transition indicator value, NIV [J.H.

Specific changes in cerebral second messenger accumulation underline REM sleep inhibition induced by the exposure to low ambient temperature.

In the rat the exposure to an ambient temperature (Ta) of -10 degrees C induces an almost total REM sleep deprivation that results in a proportional rebound in the following recovery at normal laboratory Ta when the exposure lasts for 24 h, but in a rebound much lower than expected when the exposure lasts 48 h. The possibility that this may be related to plastic changes in the nervous structures involved in the control of thermoregulation and REM sleep has been investigated by measuring changes in the concentration of adenosine 3':5'-cyclic monophosphate (cAMP) and D-myo-inositol 1,4,5-trisphosphate (IP(3)) in the preoptic-anterior hypothalamic area (PO-AH), the ventromedial hypothalamic nucleus (VMH) and, as a control, the cerebral cortex (CC). Second messenger concentration was determined in animals either stimulated by being exposed to hypoxia, a depolarizing condition that induces maximal second messenger accumulation or unstimulated, at the end of a 24-h and a 48-h exposure to -10 degrees C and also between 4 h 15 min and 4 h 30 min into recovery (early recovery).

Thermogenesis of interscapular brown adipose tissue selectively influences pontine and preoptic-hypothalamic temperatures during sleep in the rat.

The thermal influence of dorsal cervical and interscapular brown adipose tissue (ISBAT) on pontine and preoptic-hypothalamic temperatures was studied in unrestrained adult male rats across the non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM) sleep states. The animals had chronically implanted electrodes and thermistors for electroencephalographic and temperature recordings. After acclimation to either low (4 degrees C) or neutral (30 degrees C) ambient temperatures, the rats were studied before and after ISBAT excision.

Thermoregulation and sleep.

This review describes the systemic physiological phenomena characterizing the interaction between thermoregulatory and sleep processes in the adult mammal. Homeostatic thermoregulation is preserved across the behavioral states of quiet wakefulness and non-rapid eye movement sleep notwithstanding state-dependent differences in threshold and gain of effector responses to thermal loads. In many mammalian species rapid eye movement sleep is characterized by the suppression or depression of thermoregulatory responses to thermal loads.

Systemic hemodynamic changes raising brain temperature in REM sleep.

The present research studied the mechanisms underlying the increase in brain temperature during REM sleep in the unrestrained rabbit carrying chronically implanted electrodes, thermistors and common carotid artery occluders. During the ultradian wake-sleep cycle at constant ambient temperature (25+/-2 degrees C), we recorded: (i) the ear pinna temperature as an indirect indicator of blood flow affecting heat loss from the systemic heat exchangers of the head, (ii) the temperature of the pons and hypothalamus as indirect indicators of the temperature of vertebral artery blood (systemic cooling only) and carotid artery blood (both systemic and selective cooling), respectively, and (iii) the changes induced in these temperatures by short-lasting bilateral common carotid artery occlusion. The results show that during REM sleep both systemic and selective brain cooling are depressed by a spontaneous decrease in the common carotid artery blood flow and the associated autoregulatory increase in the vertebral artery share of the cerebral blood supply.