Abstract
Numerous data show a reciprocal interaction between REM sleep and thermoregulation. During REM sleep, the function of thermoregulation appears to be impaired; from the other hand, the tonic activation of thermogenesis, such as during cold exposure, suppresses REM sleep occurrence. Recently, both the central neural network controlling REM sleep and the central neural network controlling thermoregulation have been progressively unraveled. Thermoregulation was shown to be controlled by a central “core” circuit, responsible for the maintenance of body temperature, modulated by a set of accessory areas. REM sleep was suggested to be controlled by a group of hypothalamic neurons overlooking at the REM sleep generating circuits within the brainstem. The two networks overlap in a few areas, and in this review, we will suggest that in such overlap may reside the explanation of the reciprocal interaction between REM sleep and thermoregulation. Considering the peculiar modulation of thermoregulation by REM sleep the result of their coincidental evolution, REM sleep may therefore be seen as a period of transient heterothermy.
Highlights
Specialty section: This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology
The two networks overlap in a few areas, and in this review, we will suggest that in such overlap may reside the explanation of the reciprocal interaction between REM sleep and thermoregulation
A way to consider changes in the activity of median preoptic nucleus (MnPO) in rapid-eye movement sleep (REMS) deprivation and recovery (Gvilia et al, 2006; Dentico et al, 2009) is that this nucleus belongs to a preoptic set which is thought to form, with the dorso-medial hypothalamus (DMH), a visceromotor pattern generator (HVPG)
Summary
Initial studies on the interaction between sleep and thermoregulation were carried out, in different species, at both low and high Tas (Parmeggiani and Rabini, 1970; Schmidek et al, 1972; Haskell et al, 1981; Sichieri and Schmidek, 1984). Since endothermic homeotherms evolved with a Tb that was much closer to the upper than to the lower limit of their lethal core temperature, the interaction between REMS and thermoregulation has mostly been addressed within the wider span of cold defense mechanisms In the rat, this approach showed that REMS is reduced proportionally to Ta and that the REMS debt is fully recovered, following the return to TNZ, through a mechanism based on the frequency rather than the duration of episodes (Cerri et al, 2005; Amici et al, 2008). This appeared to be counteracted by behavioral thermoregulation, since deprived animals were able to select progressively higher Tas in a thermal gradient (Prete et al, 1991), but not by an increase in metabolic rate, which was concomitant with an incremental hyperphagia These results were further clarified by the finding, in REMS-deprived rats, of an increased expression of the uncoupling protein-1 in the brown adipose tissue (BAT) and a decrease in leptin secretion (Koban and Swinson, 2005). These results raise the possibility that the distinctive trait of REMS is the development of a poikilothermic condition, and this may be the reason why REMS occurrence is so intensely influenced by thermoregulation
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