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一小部分 DN1p 神经元整合热敏输入,通过 CNMa 信号促进觉醒。

A subset of DN1p neurons integrates thermosensory inputs to promote wakefulness via CNMa signaling.

机构信息

School of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, 2 Sipailou Road, Nanjing 210096, China.

CAS Key Laboratory of Brain Connectome and Manipulation, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen 518055, China.

出版信息

Curr Biol. 2021 May 24;31(10):2075-2087.e6. doi: 10.1016/j.cub.2021.02.048. Epub 2021 Mar 18.

DOI:10.1016/j.cub.2021.02.048
PMID:33740429
Abstract

Sleep is an essential and evolutionarily conserved behavior that is modulated by many environmental factors. Ambient temperature shifting usually occurs during climatic or seasonal change or travel from high-latitude area to low-latitude area that affects animal physiology. Increasing ambient temperature modulates sleep in both humans and Drosophila. Although several thermosensory molecules and neurons have been identified, the neural mechanisms that integrate temperature sensation into the sleep neural circuit remain poorly understood. Here, we reveal that prolonged increasing of ambient temperature induces a reversible sleep reduction and impaired sleep consolidation in Drosophila via activating the internal thermosensory anterior cells (ACs). ACs form synaptic contacts with a subset of posterior dorsal neuron 1 (DN1p) neurons and release acetylcholine to promote wakefulness. Furthermore, we identify that this subset of DN1ps promotes wakefulness by releasing CNMamide (CNMa) neuropeptides to inhibit the Dh44-positive pars intercerebralis (PI) neurons through CNMa receptors. Our study demonstrates that the AC-DN1p-PI neural circuit is responsible for integrating thermosensory inputs into the sleep neural circuit. Moreover, we identify the CNMa signaling pathway as a newly recognized wakefulness-promoting DN1 pathway.

摘要

睡眠是一种基本的、进化上保守的行为,受许多环境因素的调节。环境温度的变化通常发生在气候或季节变化期间,或者是动物从高纬度地区到低纬度地区的迁徙过程中,这会影响动物的生理机能。环境温度的升高会调节人类和果蝇的睡眠。尽管已经鉴定出了几个热敏分子和神经元,但将温度感觉整合到睡眠神经回路中的神经机制仍知之甚少。在这里,我们揭示了延长环境温度的升高会通过激活内部热敏前细胞 (ACs) 诱导果蝇可逆性的睡眠减少和睡眠巩固受损。ACs 与后背侧神经元 1 (DN1p) 神经元的一个亚群形成突触接触,并释放乙酰胆碱以促进觉醒。此外,我们发现这部分 DN1ps 通过释放 CNMamide (CNMa) 神经肽通过 CNMa 受体抑制 Dh44 阳性中脑间脑复合体 (PI) 神经元来促进觉醒。我们的研究表明,AC-DN1p-PI 神经回路负责将热敏感觉输入整合到睡眠神经回路中。此外,我们还发现 CNMa 信号通路是一种新发现的促进觉醒的 DN1 通路。

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