Intracellular chloride regulation mediates local sleep pressure in the cortex.
Intracellular chloride regulation mediates local sleep pressure in the cortex.
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DOI：
10.1038/s41593-022-01214-2
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发表时间：
2023-01
影响因子：
25
通讯作者：
Akerman CJ
中科院分区：
文献类型：
--
作者：
Alfonsa H;Burman RJ;Brodersen PJN;Newey SE;Mahfooz K;Yamagata T;Panayi MC;Bannerman DM;Vyazovskiy VV;Akerman CJ
长时间的清醒与表现下降和睡眠压力增加有关。在皮层中，这表现为网络活动的变化。这些变化显示出取决于清醒体验的局部变化，其潜在机制代表了克服疲劳影响的目标。在这里，我们揭示了细胞内氯调节的核心作用，它通过皮层锥体神经元中的 GABAA 受体设定突触后抑制的强度。清醒导致 GABAA 受体平衡电位的去极化变化，反映了清醒期间局部活动依赖性过程，并涉及氯协同转运蛋白活性的变化。这些变化是皮层局部睡眠压力的电生理学和行为标志的基础——包括非快速眼动睡眠期间的慢波活动水平——以及睡眠剥夺的清醒状态下的低频振荡活动和性能水平降低。这些发现表明氯调节是睡眠-觉醒历史、皮质活动和行为之间的重要联系。
Extended wakefulness is associated with reduced performance and the build-up of sleep pressure. In the cortex, this manifests as changes in network activity. These changes show local variation depending on the waking experience, and their underlying mechanisms represent targets for overcoming the effects of tiredness. Here we reveal a central role for intracellular chloride regulation, which sets the strength of postsynaptic inhibition via GABAA receptors in cortical pyramidal neurons. Wakefulness results in depolarizing shifts in the equilibrium potential for GABAA receptors, reflecting local activity-dependent processes during waking, and involving changes in chloride cotransporter activity. These changes underlie electrophysiological and behavioral markers of local sleep pressure within cortex — including the levels of slow-wave activity during non-rapid eye movement sleep — as well as low-frequency oscillatory activity and reduced performance levels in the sleep-deprived awake state. These findings identify chloride regulation as a crucial link between sleep–wake history, cortical activity and behavior.
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