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P L Parmeggiani

Publications and source records attributed to P L Parmeggiani.

At least 19 recordsLinked to original sources

REM sleep enhancement due to rhythmical auditory stimulation in the rat.

From a physiological viewpoint, REM sleep (REMS) is a period during which homeostatic physiological regulations are impaired. In the rat, REMS occurs in two forms respectively characterized by episodes separated by long intervals (single REMS episodes) and by episodes which have short intervals and occur in sequences (REMS clusters). Since the partition of REMS in the form of either single or clustered episodes may reveal how the REMS drive and body homeostatic processes interact in the control of REMS occurrence, we have used this approach to clarify the effects of the rhythmical delivery of an auditory stimulus (1000 Hz, 63 or 88 dB, 50 ms, every 20 s), which has been previously observed by different authors to enhance REMS in the absence of a previous sleep deprivation. Stimuli were delivered to pairs of animals and triggered by the occurrence of REMS in one rat (REMS-selective stimulation), whilst the other animal received the same stimulus irrespectively of the stage of the wake-sleep cycle (REMS-unselective stimulation). The results showed that the REMS-selective stimulation did not change the overall amount of REMS, since an increase in the occurrence of REMS clusters was concomitant with a decrease in the occurrence of single REMS episodes. In contrast, under the REMS-unselective stimulation, the total amount of REMS was increased during the second day of stimulation through an increase in the duration of both types of REMS episodes. Since during the REMS-unselective stimulation 87% of the stimuli fell outside REMS (i.e., during the REMS interval), the results show that the occurrence of REMS is more consistently affected when the stimuli are delivered in a period during which homeostatic physiological regulations are fully operant.

Acoustic Stimulation↗

Pattern of REM sleep occurrence in continuous darkness following the exposure to low ambient temperature in the rat.

The occurrence of REM sleep episodes, separated by intervals >3 min (single episodes) and < or =3 min (sequential episodes), was determined in the rat during the recovery (ambient temperature (Ta) 23 degrees C, L period of the LD [12 h:12 h]-cycle), which followed the exposure to low Ta (0 and -10 degrees C) during the D period of the previous LD-cycle, either in normal light (DL) or in continuous darkness (DD). Both exposures were characterized by an almost complete disappearance of REM sleep, whilst the recoveries showed an increase in the amount of REM sleep in the form of sequential episodes, which in DD was particularly prominent and concomitant with a decrease in the amount of REM sleep in the form of single episodes. The initial 2 h-rate of REM sleep occurrence was lower following the exposure to Ta -10 degrees C, than to Ta 0 degrees C. In DD, such an effect was due to the large reduction in the occurrence of sequential REM sleep episodes. A functional correlate of this finding is that the accumulation capacity of a second messenger (cAMP) was found to be lower at the end of the exposure to Ta -10 degrees C, with respect to both the control (Ta 23 degrees C) and the end of exposure to Ta 0 degrees C, in the preoptic-anterior hypothalamus, but not in the cerebral cortex.

Analysis of Variance↗

Changes in REM sleep occurrence due to rhythmical auditory stimulation in the rat.

The effects of the rhythmical delivery of an auditory stimulus (1000 Hz, from 50 to 100 dB, 20 ms, every 20 s) on the pattern of rapid eye movement (REM) sleep occurrence was studied in the rat. The stimulation was simultaneously carried out on pairs of rats over 5 consecutive days (10-h recording sessions), during which a tone of increasing intensity (50, 63, 75, 88, 100 dB) was used. In each experimental session, auditory stimulation was triggered by the REM sleep occurrence of one rat (REMS-selective stimulation) whilst the other rat simultaneously received the same stimuli, but during any stage of the wake-sleep cycle (REMS-unselective stimulation). The results showed that the total amount of REM sleep in the 10-h recording session was increased over the 5 days of stimulation in the REMS-unselective group. This effect was due to an increase in the mean duration of REM sleep episodes. However, no significant changes were observed in animals under REMS-selective stimulation, nor in a third group of animals in which the spontaneous evolution of REM sleep occurrence (REMS-spontaneous) was studied. Since 86% of the stimuli under the REMS-unselective auditory stimulation fell outside REM sleep, the result would suggest that REM sleep occurrence is affected when the stimuli are delivered during a time period (i.e. during wakefulness or non-REM sleep) in which it is well known that physiological regulations are fully operant.

Acoustic Stimulation↗

Changes in selective brain cooling across the behavioral states of the ultradian wake-sleep cycle.

In cats, the behavioral state-dependent negative correlation of the pontine-hypothalamic temperature difference, an indicator of selective brain cooling, with the hypothalamic-ear pinna temperature difference, which is an indicator of heat loss from the heat exchangers of the head, is suppressed after bilateral common carotid ligature. Behavioral state-dependent selective brain cooling may underlie a thermal feedback mechanism differentiating the relative influences of hypothalamic and extra-hypothalamic thermoreceptors on the thermoregulatory system during quiet wakefulness and NREM sleep.

Animals↗

Selective brain cooling is impaired in REM sleep.

There are systemic and selective mechanisms for brain cooling in mammals. The difference between the temperatures of the vertebral and the carotid blood perfusing the brain is determined by selective heat loss and is, therefore, a quantitative indicator of the intensity of selective brain cooling. Across the wake-sleep cycle systemic and selective brain cooling are affected by state-dependent autonomic changes. In REM sleep selective brain cooling is impaired.

Animals↗

Control of REM sleep: an aspect of the regulation of physiological homeostasis.

Since REM sleep is characterized by a suspension of the hypothalamic integration of homeostatic regulations, it has been assumed that the duration of both REM sleep episodes and of the time interval between the end of one episode and the beginning of the following episode may be regulated according to sleep related processes and the homeostatic needs of the organism. A series of studies performed on the rat has shown that REM sleep episodes occur as two basic types: single REM sleep episodes, that are separated by intervals > 3 min and sequential episodes, that are separated by intervals < or = 3 min and appear in a cluster. Moreover, it has been observed that, in this species, a change in REM sleep occurrence is caused by a modification in the number of episodes and not in their duration. With respect to this, sleep deprivation and recovery are characterized by a decrease and an increase, respectively, in the number of sequential REM sleep episodes, but the number of single episodes tends to be kept constant. The central aspects of this kind of regulation have been examined biochemically in the preoptic-anterior hypothalamus, an area involved in the control of autonomic and sleep related processes. The results show that the accumulation of adenosine 3':5'-cyclic monophosphate (cAMP) is impaired, in this region, during sleep deprivation and appears to return to the control levels, during the recovery, with a rate inversely related to the degree of the previous deprivation. Moreover, it has been observed that the systemic administration of DL-propranolol and LiCl reduces cAMP accumulation mainly in the preoptic-anterior hypothalamus; this condition is concomitant with a reduction in REM sleep occurrence.

Animals↗

The influence of a heavy thermal load on REM sleep in the rat.

This study was carried out in order to further test the hypothesis that the occurrence of REM sleep in the rat in the form of episodes separated by long intervals (single REM sleep episodes) and by short intervals (sequential REM sleep episodes) is differently influenced by changes in both sleep and ambient related processes. Rats were studied during the exposure to Ta -10 degrees C for 24 or 48 h and during a 12 h recovery period at laboratory Ta (23 degrees C) following either the first or the second 24 h of cold exposure. The exposure to such a low Ta induced an almost complete abolition of REM sleep which was followed, during recovery, by a marked REM sleep rebound. However, in spite of the larger REM sleep deprivation, the REM sleep rebound was weaker following the 48 h-exposure than that following the exposure for 24 h. The increase in the amount of REM sleep during the recovery period was due to an increase in the amount of that occurring in the form of sequential episodes, whilst that in the form of single episodes did not change with respect to control levels. However, the occurrence of REM sleep in the form of sequential episodes was partially impaired during the REM sleep rebound observed in the recovery period following the 48 h-exposure. These results would suggest that the homeostatic regulation of physiological variables may conflict with that of REM sleep occurrence and that the degree of such a contrast is indicated, at low Ta, by the amount of REM sleep in the form of single episodes and, during the following recovery, by the amount of REM sleep in the form of sequential episodes.

Animals↗

A pontine-hypothalamic temperature difference correlated with cutaneous and respiratory heat loss.

The role of cutaneous and respiratory heat loss for selective brain cooling in different species is discussed and new experimental results from a comparative study are summarized. In three species (cat, rabbit and rat) the difference between pontine and hypothalamic temperatures was studied as a function of head heat exchanger vasomotion appraised by the difference between hypothalamic and ear pinna (cats and rabbits) or nasal mucosa (rats) temperatures during the behavioral states of wakefulness and slow wave sleep at an ambient temperature of 24+/-1 degrees C. The results show that: (i) the pontine-hypothalamic temperature difference is an useful indicator of selective brain cooling since it is positive and inversely correlated with the hypothalamic-ear pinna temperature difference in cats and rabbits and with the hypothalamic-nasal mucosa temperature difference in rats; (ii) respiratory heat loss prevails quantitatively over cutaneous heat loss in maintaining this difference.

Animals↗

The capacity to accumulate cyclic AMP in the preoptic-anterior hypothalamic area of the rat is affected by the exposition to low ambient temperature and the subsequent recovery.

The accumulation of adenosine 3':5'-cyclic monophosphate (cAMP) was measured in the preopticanterior hypothalamic area, the cerebral cortex, and the hippocampus of rats exposed to different ambient temperatures: (1) 23 +/- 0.5 degrees C, for 53 h +/- 20 min (control); (2) -10 +/- 1 degrees C, for 53 h +/- 20 min (exposure to low ambient temperature); (3) -10 degrees C for 48 h and 23 degrees C for the following 5 h +/- 20 min (recovery). The capacity to accumulate cAMP was tested by subjecting animals to acute hypoxia, a stimulus which is known to induce a large increase in brain cAMP concentration. In the control condition, hypoxic stimulation increases cAMP concentration in all the brain regions studied. In contrast, during the exposure to low ambient temperature, whilst both the cerebral cortex and the hippocampus show the same levels of accumulation found in the control condition, cAMP accumulation is reduced in the preoptic-anterior hypothalamic area. However, during the first few hours of the recovery period, the preoptic-anterior hypothalamic area is able to reattain the capacity for cAMP accumulation observed in the control condition.

Animals↗

cAMP accumulation in the hypothalamus, cerebral cortex, pineal gland and brown fat across the wake-sleep cycle of the rat exposed to different ambient temperatures.

The concentration of adenosine 3':5' cyclic monophosphate (cAMP) was determined in the anteroventro-medial hypothalamus, the cerebral cortex, the pineal gland and the interscapular brown adipose tissue, during the different stages of the wake-sleep cycle of rats kept, under a 12-12-h light-dark cycle, in different environmental conditions, i.e., control (47-52 h at ambient temperature (Ta) 23 +/- 0.5 degrees C), exposure (47-52 h at Ta 0 +/- 1 degree C) and recovery (1-4 h at Ta 23 degrees C after 48 h at Ta 0 degree C). The results show that cAMP concentration consistently changed: (1) during the wake-sleep cycle in the anteroventro-medial hypothalamus, decreasing from wakefulness to sleep; (2) during the dark-light transition in the pineal gland, increasing with the onset of the light phase; and (3) with the environmental condition in the interscapular brown adipose tissue increasing, with respect to the control condition, in exposure and recovery. No significant changes in cAMP concentration were observed in the cerebral cortex.

Adipose Tissue, Brown↗

Postural and sympathetic influences on brain cooling during the ultradian wake-sleep cycle.

The influence of posture and tonic vasoconstrictor sympathetic outflow on systemic (ear pinna-environment) and selective (carotid rete-venous plexus) heat exchange underlying brain cooling was studied in cats chronically implanted with EEG and EMG electrodes, and transducers that measured hypothalamic, pontine and ear pinna temperatures across the ultradian wake-sleep cycle in a thermoneutral environment. Transmural pressure on heat exchanger vasculature was varied by keeping the animal's head above or at heart level. The vasoconstrictor sympathetic outflow to heat exchanger vasculature was varied both by keeping the animal's abdomen cool or warm and by means of bilateral common carotid ligature. The results show that a rise in transmural pressure enhances selective brain cooling and weakens systemic brain cooling. An increase in tonic vasoconstrictor sympathetic outflow decreases both systemic and selective brain cooling.

Activity Cycles↗

Responses of extrahypothalamic neurons to short temperature transients during the ultradian wake-sleep cycle.

The thermosensitivity of neurons in thalamo-striate-limbic structures located dorsally to the classical thermosensitive anterior hypothalamic-preoptic region was studied in cats during the natural ultradian wake-sleep cycle. Direct cooling or warming of the brain tissue by means of water-perfused thermodes was combined with tonic cooling or warming of the abdominal wall using a water-perfused heat exchanger on which the animal was lying. Out of 482 neurons, 116 (24.1%) were thermosensitive. They were located in the nuclei reticularis and ventralis anterior of the thalamus, the fundus of the caudate nucleus, the bed nucleus of the stria terminalis, the bed nucleus of the inferior thalamic peduncle, and the nucleus of the anterior commissure. Abdominal warming increased the effect of direct brain warming and decreased the effect of direct brain cooling; opposite effects were obtained by abdominal cooling. Thermosensitivity was present during wakefulness and synchronized sleep, but depressed or altered during desynchronized sleep.

Abdominal Muscles↗

Hypothalamic homeothermy across the ultradian sleep cycle.

In the ambient thermal zone for the vasomotor regulation of body temperature hypothalamic temperature changes across the states of the ultradian sleep cycle are the result of state-dependent heat production-heat loss imbalances affecting the temperature of the arterial blood perfusing the brain. However, the changes in arterial blood temperature are efficiently buffered, at a low energetic cost, by the thermal inertia of the mass of body water. Thus, the oscillations in hypothalamic temperature are maintained within a width of a few tenths of a degree and are so small as to be subliminal as thermal feedback stimuli for thermoregulatory responses. This passive hypothalamic homeothermy would support the hypothesis that a phylogenetic pressure was operative early on in mammals in order to limit the duration of the ultradian sleep cycle so as to fit the thermal inertia of the different masses of body water in mammals of different sizes.

Activity Cycles↗

Mechanisms underlying hypothalamic temperature changes during sleep in mammals.

The mechanisms underlying hypothalamic temperature (Thy) changes across the ultradian wake-sleep cycle were analyzed in cats chronically implanted with EEG and EMG electrodes, and transducers that measured Thy and pontine temperature (Tp). The influence of artificially induced changes in (i) systemic blood temperature, (ii) heat loss from the specific heat exchangers of the head, and (iii) carotid artery occlusion, on Thy, Tp and ear pinna temperature (Ts) during waking (W), synchronized sleep (SS) and desynchronized sleep (DS) were assessed in animals maintained in a thermoneutral environment. The results show that the decrease in Thy during SS is dependent on increased heat loss from heat exchangers (ear pinna), whereas the increase in Thy during DS is due to an alteration in the arterial blood perfusion of the circle of Willis receiving an increased supply of warm vertebral blood that replaces a decrease in supply of cool carotid blood.

Activity Cycles↗

Cold-defense function of brown adipose tissue during sleep.

Rats with chronically implanted electroencephalograph scalp electrodes and thermistors were exposed to 24 and 4 degrees C ambient temperatures during the light hours before and after acclimation to 4 degrees C ambient temperature for 9 days. During synchronized sleep, deep interscapular temperature was higher at 4 degrees C than at 24 degrees C both before and after acclimation to cold. After ablation of brown adipose tissue, deep interscapular temperature was lower at 4 degrees C than at 24 degrees C during synchronized sleep. In the presence of brown adipose tissue, deep interscapular temperature decreased sharply during desynchronized sleep at 4 degrees C both before and after acclimation to cold. This decrease was subsequent to and correlated with an increase in the temperature of the nasal mucosa. The decrease in deep interscapular temperature during desynchronized sleep at 4 degrees C ambient temperature was markedly reduced by ablation of the interscapular brown adipose tissue.

Acclimatization↗