Nitric Oxide Synthase Neurons in the Preoptic Hypothalamus Are NREM and REM Sleep-Active and Lower Body Temperature

Frontiers in Neuroscience

Bryan Hsieh²  Raquel Yustos³  Wei Ba³  Xiao Yu³  Leda Lignos³  Reesha Zahir³  Alexei L. Vyssotski⁴  Timothy G. Constandinou⁵  William Wisden⁶  Nicholas P. Franks⁶  Edward C. Harding⁷  Florian T. Merkle⁷ 

[1] Centre for Neurotechnology, Imperial College London, London, United Kingdom;Department of Electrical and Electronic Engineering, Imperial College London, London, United Kingdom;Department of Life Sciences, Imperial College London, London, United Kingdom;Institute of Neuroinformatics, University of Zürich/ETH Zürich, Zurich, Switzerland;United Kingdom Dementia Research Institute Care Research and Technology, Imperial College London, London, United Kingdom;United Kingdom Dementia Research Institute at Imperial College London, London, United Kingdom;Wellcome-MRC Institute of Metabolic Science and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, United Kingdom;

关键词: preoptic hypothalamus;    nitric oxide;    sleep;    calcium photometry;    body temperature;    tetanus-toxin light-chain;   

DOI  :  10.3389/fnins.2021.709825

来源: DOAJ

【 摘 要 】

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM and REM active, especially at the boundary of wake to NREM transitions, and in the later parts of REM bouts, with lower activity during wakefulness. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 h, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically blocked MnPO/MPO NOS1 neurons were also warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

【 授权许可】

Unknown