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      The Temperature Dependence of Sleep

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          Abstract

          Mammals have evolved a range of behavioural and neurological mechanisms that coordinate cycles of thermoregulation and sleep. Whether diurnal or nocturnal, sleep onset and a reduction in core temperature occur together. Non-rapid eye movement (NREM) sleep episodes are also accompanied by core and brain cooling. Thermoregulatory behaviours, like nest building and curling up, accompany this circadian temperature decline in preparation for sleeping. This could be a matter of simply comfort as animals seek warmth to compensate for lower temperatures. However, in both humans and other mammals, direct skin warming can shorten sleep-latency and promote NREM sleep. We discuss the evidence that body cooling and sleep are more fundamentally connected and that thermoregulatory behaviours, prior to sleep, form warm microclimates that accelerate NREM directly through neuronal circuits. Paradoxically, this warmth might also induce vasodilation and body cooling. In this way, warmth seeking and nesting behaviour might enhance the circadian cycle by activating specific circuits that link NREM initiation to body cooling. We suggest that these circuits explain why NREM onset is most likely when core temperature is at its steepest rate of decline and why transitions to NREM are accompanied by a decrease in brain temperature. This connection may have implications for energy homeostasis and the function of sleep.

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          VTA dopaminergic neurons regulate ethologically relevant sleep-wake behaviors.

          Dopaminergic ventral tegmental area (VTA) neurons are critically involved in a variety of behaviors that rely on heightened arousal, but whether they directly and causally control the generation and maintenance of wakefulness is unknown. We recorded calcium activity using fiber photometry in freely behaving mice and found arousal-state-dependent alterations in VTA dopaminergic neurons. We used chemogenetic and optogenetic manipulations together with polysomnographic recordings to demonstrate that VTA dopaminergic neurons are necessary for arousal and that their inhibition suppresses wakefulness, even in the face of ethologically relevant salient stimuli. Nevertheless, before inducing sleep, inhibition of VTA dopaminergic neurons promoted goal-directed and sleep-related nesting behavior. Optogenetic stimulation, in contrast, initiated and maintained wakefulness and suppressed sleep and sleep-related nesting behavior. We further found that different projections of VTA dopaminergic neurons differentially modulate arousal. Collectively, our findings uncover a fundamental role for VTA dopaminergic circuitry in the maintenance of the awake state and ethologically relevant sleep-related behaviors.
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            How (and why) the immune system makes us sleep.

            Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value.
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              Galanin neurons in the medial preoptic area govern parental behavior

              Mice display robust, stereotyped behaviors toward pups: virgin males typically attack pups, while virgin females and sexually experienced males and females display parental care. We show here that virgin males genetically impaired in vomeronasal sensing do not attack pups and are parental. Further, we uncover a subset of galanin-expressing neurons in the medial preoptic area (MPOA) that are specifically activated during male and female parenting, and a different subpopulation activated during mating. Genetic ablation of MPOA galanin neurons results in dramatic impairment of parental responses in males and females and affects male mating. Optogenetic activation of these neurons in virgin males suppresses inter-male and pup-directed aggression and induces pup grooming. Thus, MPOA galanin neurons emerge as an essential regulatory node of male and female parenting behavior and other social responses. These results provide an entry point to a circuit-level dissection of parental behavior and its modulation by social experience.
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                Author and article information

                Contributors
                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                24 April 2019
                2019
                : 13
                : 336
                Affiliations
                [1] 1Department of Life Sciences, Imperial College London , London, United Kingdom
                [2] 2Centre for Neurotechnology, Imperial College London , London, United Kingdom
                [3] 3UK Dementia Research Institute, Imperial College London , London, United Kingdom
                Author notes

                Edited by: Yu Hayashi, University of Tsukuba, Japan

                Reviewed by: Genshiro A. Sunagawa, RIKEN Center for Biosystems Dynamics Research, Japan; Ramalingam Vetrivelan, Beth Israel Deaconess Medical Center, Harvard Medical School, United States

                *Correspondence: Nicholas P. Franks, n.franks@ 123456imperial.ac.uk William Wisden, w.wisden@ 123456imperial.ac.uk

                This article was submitted to Sleep and Circadian Rhythms, a section of the journal Frontiers in Neuroscience

                Article
                10.3389/fnins.2019.00336
                6491889
                31105512
                66fd5ad7-2eb0-480f-9a22-c2ce4684e043
                Copyright © 2019 Harding, Franks and Wisden.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 15 January 2019
                : 22 March 2019
                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 159, Pages: 16, Words: 0
                Funding
                Funded by: Wellcome Trust 10.13039/100004440
                Categories
                Neuroscience
                Review

                Neurosciences
                sleep-wake cycle,thermoregulation,thermoregulatory behaviour,circadian,preoptic area,anterior hypothalamus,energy balance,nesting

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