Biomedical subjects

Pier Luigi Parmeggiani

Publications and source records attributed to Pier Luigi Parmeggiani.

6 recordsLinked to original sources

PubMed2005

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. SETTING: Laboratory of Physiological Regulation during the Wake-Sleep Cycle, Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna. SUBJECTS: Twenty-four male albino rats. INTERVENTIONS: Animals were implanted with electrodes for electroencephalographic recording and a thermistor for measuring hypothalamic temperature. MEASUREMENTS AND RESULTS: Wake-sleep stage duration and the electroencephalographic spectral analysis performed by fast Fourier transform were compared among baseline, exposure, and recovery conditions. The amount of non-rapid eye movement sleep was slightly depressed by cold exposure, but no rebound was observed during the recovery period. Delta power during non-rapid eye movement sleep was decreased in animals exposed to the lowest ambient temperatures and increased during the first day of the recovery. In contrast, rapid eye movement sleep was greatly depressed by cold exposure and showed an increase during the recovery. Both of these effects were dependent on the ambient temperature of the exposure. Moreover, theta power was increased during rapid eye movement sleep in both the exposure and the first day of the recovery. CONCLUSION: These findings show that sleep-stage duration and electroencephalogram power are simultaneously affected by cold exposure. The effects on rapid eye movement sleep appear mainly as changes in the duration, whereas those on non-rapid eye movement sleep are shown by changes in delta power. These effects are temperature dependent, and the decrease of both parameters during the exposure is reciprocated by an increase in the subsequent recovery.

Animals↗

PubMed2004

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). At the end of both exposure conditions, cAMP concentration significantly decreased in PO-AH-VMH, but did not change in CC, whilst changes in IP(3) concentration were similar in all these regions. The low cAMP concentration in PO-AH-VMH was concomitant with a significantly low accumulation in hypoxia. The normal capacity of cAMP accumulation was only restored in the early recovery following 24 h of exposure, but not following 48 h of exposure, suggesting that this may be a biochemical equivalent of the REM sleep inhibition observed during 48 h of exposure and which is carried over to the recovery.

Animals↗

PubMed2004

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. The warming influence of ISBAT thermogenesis activated by low ambient temperature reached the pontine and the preoptic-hypothalamic areas. ISBAT thermogenesis is necessary to maintain the homeothermy of the preoptic-hypothalamic area in NREM sleep at low ambient temperature. Such an ISBAT thermal effect may contribute to the integrated control of non-shivering and shivering thermogenesis.

Adipose Tissue, Brown↗

PubMed2003

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. In human adults, however, rapid eye movement sleep is not as thermally altered as in other mammals. The experimental evidence shows that the interaction between thermoregulatory and sleep processes occurs at the level of the preoptic-hypothalamic thermostat. A main open question concerns the nature of the over-riding demand imposing on the central nervous system the temporary suspension of homeostatic integrative regulation in rapid eye movement sleep.

Animals↗

PubMed2002

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.

Activity Cycles↗

PubMedDate not supplied

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. Benington et al., Sleep 17 (1994) 28-36]. However, such transitions are not always followed by a REMS episode, but are often followed by an awakening. In the present study, the relationship between changes in EEG activity and hypothalamic temperature (Thy), taken as an index of autonomic activity, was studied within a window consisting of the 60s which precedes a state change from a consolidated NREMS episode. Furthermore, the probability that a transition would lead to REMS or wake was analysed. The results showed that, within this time window, both a modified NIV (NIV(60)) and the difference between Thy at the limits of the window (Thy(D)) were related to the probability of REMS onset. Both the relationship between the indices and the probability of REMS onset was sigmoid, the latter of which saturated at a probability level around 50-60%. The efficacy for the prediction of successful transitions from NREMS to REMS found using Thy(D) as an index supports the view that such a transition is a dynamic process where the physiological risk to enter REMS is weighted at a central level.

Activity Cycles↗