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Review
. 2018 May 1;33(3):182-196.
doi: 10.1152/physiol.00007.2018.

Is Adenosine Action Common Ground for NREM Sleep, Torpor, and Other Hypometabolic States?

Alessandro Silvani  1 , Matteo Cerri  1   2 , Giovanna Zoccoli  1 , Steven J Swoap  3
Affiliations
Review

Is Adenosine Action Common Ground for NREM Sleep, Torpor, and Other Hypometabolic States?

Alessandro Silvani et al. Physiology (Bethesda). .

Abstract

This review compares two states that lower energy expenditure: non-rapid eye movement (NREM) sleep and torpor. Knowledge on mechanisms common to these states, and particularly on the role of adenosine in NREM sleep, may ultimately open the possibility of inducing a synthetic torpor-like state in humans for medical applications and long-term space travel. To achieve this goal, it will be important, in perspective, to extend the study to other hypometabolic states, which, unlike torpor, can also be experienced by humans.

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Figures

FIGURE 1.
FIGURE 1.
Qualitative comparison of physiological variables and behavior between NREM sleep and natural torpor NREM, non-rapid eye movement; Tb, body temperature; A1R and A2aR, adenosine receptors type 1 and 2a, respectively.
FIGURE 2.
FIGURE 2.
Common and disparate neural structures potentially involved in NREM sleep and torpor The figure shows neural structures that, based on the available evidence, are potentially involved in NREM sleep and torpor. Cf. the text for details and references. A: the brain structures are shown on a sagittal section of the mouse brain and marked in color code: red and yellow circles, structures thought to be involved only in NREM sleep and torpor, respectively; yellow circles with red rim, structures potentially involved both in NREM sleep and in torpor. This grouping is emphasized in B, where the same brain structures are inscribed in Venn diagrams corresponding to the NREM sleep and torpor structure sets. nNOS nn, sleep-active cortical neurons containing both gamma-amino-butyric acid (GABA) and neuronal nitric oxide synthase (nNOS); BF, basal forebrain; MPO, hypothalamic medial preoptic area; MnPO, VLPO, SCN, ARC, PVN, and DMH, hypothalamic median preoptic, ventrolateral preoptic, suprachiasmatic, arcuate, paraventricular, and dorsomedial nuclei, respectively; PB, parabrachial nucleus; PPT, pedunculopontine nucleus; RPa, raphe pallidus; PZ, parafacial zone; NTS, nucleus of the solitary tract.
FIGURE 3.
FIGURE 3.
Diagram indicating postulated central pathways mediating autonomic changes during NREM sleep The broken lines indicate indirect connections, including one or more relay nuclei. Namb/DMNX, nucleus ambiguous/dorsal motor nucleus of the vagus nerve. Figure was modified from Ref , with permission from the American Physiological Society.
FIGURE 4.
FIGURE 4.
Circadian and sleep-related control of autonomic and metabolic factors that may modulate torpor CLOCK, BMAL1, CRY, and PER, key proteins coded by homonymous core clock genes; AMP and ADP, adenosine mono- and diphosphate, respectively; NAD+, oxidized nicotinamide adenine dinucleotide.
FIGURE 5.
FIGURE 5.
Sources of adenosine potentially involved in the control of NREM sleep and torpor SAH, S-adenosylhomocysteine; ENT1, equilibrative nucleoside transporter 1. Cf. the text for details and references.
FIGURE 6.
FIGURE 6.
Qualitative comparison of physiological variables and behavior between synthetic torpor induced by A1R activation vs. raphe pallidus inhibition Tb, body temperature; A1R, adenosine receptors.
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