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首页> 外文期刊>Nature Communications >Galanin neurons in the ventrolateral preoptic area promote sleep and heat loss in mice
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Galanin neurons in the ventrolateral preoptic area promote sleep and heat loss in mice

机译:腹侧前视区的甘丙肽神经元促进小鼠睡眠和热量流失

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The preoptic area (POA) is necessary for sleep, but the fundamental POA circuits have remained elusive. Previous studies showed that galanin (GAL)- and GABA-producing neurons in the ventrolateral preoptic nucleus (VLPO) express cFos after periods of increased sleep and innervate key wake-promoting regions. Although lesions in this region can produce insomnia, high frequency photostimulation of the POAGAL neurons was shown to paradoxically cause waking, not sleep. Here we report that photostimulation of VLPOGAL neurons in mice promotes sleep with low frequency stimulation (1–4?Hz), but causes conduction block and waking at frequencies above 8?Hz. Further, optogenetic inhibition reduces sleep. Chemogenetic activation of VLPOGAL neurons confirms the increase in sleep, and also reduces body temperature. In addition, chemogenetic activation of VLPOGAL neurons induces short-latency sleep in an animal model of insomnia. Collectively, these findings establish a causal role of VLPOGAL neurons in both sleep induction and heat loss.
机译:视前区(POA)是睡眠所必需的,但基本的POA电路仍然难以捉摸。先前的研究表明,腹侧前视神经核(VLPO)中产生甘丙肽(GAL)和GABA的神经元在睡眠增加并支配关键的促觉区域后表达cFos。尽管该区域的病变可引起失眠,但POAGAL神经元的高频光刺激显示出反常的原因,导致醒来,而非睡眠。在这里,我们报道小鼠的VLPOGAL神经元的光刺激可通过低频刺激(1-4?Hz)促进睡眠,但会导致传导阻滞并在8?Hz以上的频率醒来。此外,光遗传学抑制作用会减少睡眠。 VLPOGAL神经元的化学生成激活证实了睡眠的增加,并且还降低了体温。此外,在失眠动物模型中,VLPOGAL神经元的化学激活可诱导短时睡眠。总的来说,这些发现建立了VLPOGAL神经元在睡眠诱导和热量损失中的因果作用。

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