Elevated excitability of Hcrt neurons with depolarized RMPs and adaptive up-regulation of prepro-Hcrt mRNA expression converge to drive sleep/wake instability in the aged brain with substantial Hcrt neuron loss. Hyperexcitable aged Hcrt neurons express functional impairment of KCNQ2/3 channel–mediated M-current and an anatomical loss of KCNQ2, compromising the neurons to repolarize.
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