Central AMPK contributes to sleep homeostasis in mice
Central AMPK contributes to sleep homeostasis in mice
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DOI：
10.1016/j.neuropharm.2009.07.015
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发表时间：
2009-09-01
影响因子：
4.7
通讯作者：
Sei, Hiroyoshi
中科院分区：
文献类型：
--
作者：
Chikahisa, Sachiko;Fujiki, Nobuhiro;Sei, Hiroyoshi
AMP激活的蛋白激酶(AMPK)是一种能量敏感的分子信号，参与糖脂代谢。已知的睡眠与能量代谢的相互作用使我们研究中枢AMPK在睡眠动态平衡中的作用。睡眠剥夺(SD)6h后，下丘脑p-AMPK蛋白表达增加，AMPK激活剂钙/钙调素依赖性蛋白激酶β(CAMKK2)和AMPK下游信号因子肉碱棕榈酰基转移酶1(CPT1)的mRNA水平也升高。中枢注射AMPK抑制剂C(CC)可抑制NREM睡眠时的EEG Delta功率，而AMPK激活剂5-氨基咪唑-4-甲酰胺核苷(AICAR)可增强EEG Delta功率。CC和AICAR均可减弱SD后NREM睡眠中Delta功率的反弹反应。这些结果表明，中枢AMPK参与了睡眠深度和睡眠内稳态的调节。(C)2009爱思唯尔有限公司。保留所有权利。
AMP-activated protein kinase (AMPK) is an energy-sensing molecular signal involved in glucose and lipid metabolism. The known interaction of sleep with energy metabolism led us to investigate the role of central AMPK in sleep homeostasis. Sleep deprivation (SD) for 6 h increased p-AMPK protein in the hypothalamus and also increased the mRNA level of Ca2+-/calmodulin (CaM)-dependent protein kinase kinase beta (CaMKK2), an activator of AMPK, and carnitine palmitoyltransferase 1 (CPT1), a downstream signaling factor of AMPK. Central injection of compound C (CC), an inhibitor of AMPK, suppressed EEG delta power during NREM sleep, while 5-aminoimidazole-4-carboxamide riboside (AICAR), an activator of AMPK, enhanced EEG delta power. The treatment of both CC and AICAR attenuated rebound responses of delta power in NREM sleep after SD. These results indicate that central AMPK is involved in the regulation of sleep depth and sleep homeostasis. (C) 2009 Elsevier Ltd. All rights reserved.