果蝇睡眠中光诱导觉醒的昼夜节律门控。

IF 1.8 4区 医学 Q3 GENETICS & HEREDITY Journal of neurogenetics Pub Date : 2023-03-01 DOI:10.1080/01677063.2022.2151596
Hoyeon Lee, Chunghun Lim
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引用次数: 1

摘要

昼夜节律和睡眠稳态构成了日常睡眠调节的双过程模型。然而,昼夜节律控制睡眠-觉醒周期的证据相对较短,因为无生物钟动物通常表现出与野生型动物相当的睡眠行为。在这里,我们研究了果蝇在不同的光-暗制度下的睡眠行为,并证明昼夜节律钟控制了光诱导的觉醒。表达酪氨酸脱羧酶2 (TDC2)的神经元的基因兴奋在夜间更明显地抑制睡眠,引起夜间活动。唤醒效应可能部分是由来自章鱼胺能神经元的谷氨酸传递介导的,并且基本上被光线掩盖。T12周期(6小时光照:6小时黑暗)的应用进一步表明,TDC2神经元的光敏效应依赖于一天中的时间。特别是,通过视觉输入通路的光感导致主观夜晚强烈的睡眠抑制,而这种效应在无时钟突变体中消失。转基因图谱显示,光诱导的觉醒和自由运行的行为节律需要不同的昼夜节律起搏器神经元群。这些结果提供了令人信服的证据,表明睡眠的昼夜节律控制是由专门用于光诱导唤醒的时钟神经元介导的。
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Circadian gating of light-induced arousal in Drosophila sleep.

Circadian rhythms and sleep homeostasis constitute the two-process model for daily sleep regulation. However, evidence for circadian control of sleep-wake cycles has been relatively short since clock-less animals often show sleep behaviors quantitatively comparable to wild-type. Here we examine Drosophila sleep behaviors under different light-dark regimes and demonstrate that circadian clocks gate light-induced arousal. Genetic excitation of tyrosine decarboxylase 2 (TDC2)-expressing neurons suppressed sleep more evidently at night, causing nocturnal activity. The arousal effects were likely mediated in part by glutamate transmission from the octopaminergic neurons and substantially masked by light. Application of T12 cycles (6-h light: 6-h dark) further showed that the light-sensitive effects of TDC2 neurons depended on the time of the day. In particular, light-sensing via visual input pathway led to strong sleep suppression at subjective night, and such an effect disappeared in clock-less mutants. Transgenic mapping revealed that light-induced arousal and free-running behavioral rhythms require distinct groups of circadian pacemaker neurons. These results provide convincing evidence that circadian control of sleep is mediated by the dedicated clock neurons for light-induced arousal.

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来源期刊
Journal of neurogenetics
Journal of neurogenetics 医学-神经科学
CiteScore
4.40
自引率
0.00%
发文量
13
审稿时长
>12 weeks
期刊介绍: The Journal is appropriate for papers on behavioral, biochemical, or cellular aspects of neural function, plasticity, aging or disease. In addition to analyses in the traditional genetic-model organisms, C. elegans, Drosophila, mouse and the zebrafish, the Journal encourages submission of neurogenetic investigations performed in organisms not easily amenable to experimental genetics. Such investigations might, for instance, describe behavioral differences deriving from genetic variation within a species, or report human disease studies that provide exceptional insights into biological mechanisms
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