Demonstrating an age-dependent mechanism underlying sleep disruption, a new Science study finds that hyperexcitable arousal circuits in the brain drive disrupted sleep in aging mice. The findings pave the way for new, targeted strategies and therapeutics.
In humans, the deterioration of sleep quality during aging is one of the most prevalent complaints. In an animal model, Li. found that aging correlated with enhanced spontaneous activity of wake-promoting brain areas during sleep . Hypocretin-expressing neurons were more active during sleep, raising the chances of brief arousals and thus causing sleep to be more fragmented.
In this study, we investigated whether the intrinsic excitability of Hcrt neurons is altered, leading to a destabilized control of sleep/wake states during aging.Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations.
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