饥饿引起的睡眠抑制需要果蝇的大脑营养传感器。

IF 1.8 4区 医学 Q3 GENETICS & HEREDITY
Yangkyun Oh, Greg S B Suh
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引用次数: 2

摘要

动物在饥饿的情况下会增加运动活动,减少睡眠时间。这表明睡眠和代谢状态是密切相关的。果蝇大脑中的营养和饥饿传感器,包括利尿激素44 (DH44)-、CN-和表达纸杯蛋糕的神经元,检测内部环境中的循环葡萄糖水平,调节胰岛素和胰高血糖素的分泌,促进食物消耗。已知食物剥夺会减少睡眠时间,但营养和饥饿传感器在调节睡眠和运动活动中的潜在作用尚不清楚。在这里,我们发现DH44神经元参与调节饥饿诱导的睡眠抑制,但CN神经元或纸杯蛋糕神经元可能不参与调节饥饿诱导的睡眠抑制或基线睡眠模式。在进食条件下,DH44神经元的失活导致正常的日常睡眠时间和模式,而在饥饿条件下,它会减少睡眠。CN神经元或纸杯蛋糕神经元被认为是果蝇大脑中的营养和饥饿传感器,它们的失活在喂食和饥饿条件下都不会影响睡眠模式。我们认为葡萄糖感知DH44神经元在介导饥饿引起的睡眠减少中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Starvation-induced sleep suppression requires the Drosophila brain nutrient sensor.

Animals increase their locomotion activity and reduce sleep duration under starved conditions. This suggests that sleep and metabolic status are closely interconnected. The nutrient and hunger sensors in the Drosophila brain, including diuretic hormone 44 (DH44)-, CN-, and cupcake-expressing neurons, detect circulating glucose levels in the internal milieu, regulate the insulin and glucagon secretion and promote food consumption. Food deprivation is known to reduce sleep duration, but a potential role mediated by the nutrient and hunger sensors in regulating sleep and locomotion activity remains unclear. Here, we show that DH44 neurons are involved in regulating starvation-induced sleep suppression, but CN neurons or cupcake neurons may not be involved in regulating starvation-induced sleep suppression or baseline sleep patterns. Inactivation of DH44 neurons resulted in normal daily sleep durations and patterns under fed conditions, whereas it ablated sleep reduction under starved conditions. Inactivation of CN neurons or cupcake neurons, which were proposed to be nutrient and hunger sensors in the fly brain, did not affect sleep patterns under both fed and starved conditions. We propose that the glucose-sensing DH44 neurons play an important role in mediating starvation-induced sleep reduction.

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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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