title: Specific changes in cerebral second messenger accumulation underline REM sleep inhibition induced by the exposure to low ambient temperature.
abstract: 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.
authors.affiliation: Dipartimento di Fisiologia umana e generale, Università di Bologna, Piazza di Porta San Donato 2, 40127 Bologna (BO), Italy. gzamboni@biocfarm.unibo.it
authors.forename: Giovanni
authors.initials: G
authors.lastname: Zamboni
authors.forename: Christine Ann
authors.initials: CA
authors.lastname: Jones
authors.forename: Rosa
authors.initials: R
authors.lastname: Domeniconi
authors.forename: Roberto
authors.initials: R
authors.lastname: Amici
authors.forename: Emanuele
authors.initials: E
authors.lastname: Perez
authors.forename: Marco
authors.initials: M
authors.lastname: Luppi
authors.forename: Matteo
authors.initials: M
authors.lastname: Cerri
authors.forename: Pier Luigi
authors.initials: PL
authors.lastname: Parmeggiani
mesh_terms: D000818:Animals; D001833:Body Temperature Regulation / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D001923:Brain Chemistry; D015220:Calcium Channels / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D053496:Inositol 1,4,5-Trisphosphate Receptors; D007295:Inositol Phosphates / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology*; D012892:Sleep Deprivation / Q000378:metabolism; D012895:Sleep, REM / Q000502:physiology*; D013997:Time Factors
chemical_list: D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D007295:Inositol Phosphates; D018160:Receptors, Cytoplasmic and Nuclear; D000242:Cyclic AMP