Prefrontal cortical regulation of REM sleep

Rapid eye movement (REM) sleep is accompanied by intense cortical activity, underlying its wake-like electroencephalogram. The neural activity inducing REM sleep is thought to originate from subcortical circuits in brainstem and hypothalamus. However, whether cortical neurons can also trigger REM sleep has remained unknown. Here we show in mice that the medial prefrontal cortex (mPFC) strongly promotes REM sleep. Bidirectional optogenetic manipulations demonstrate that excitatory mPFC neurons promote REM sleep through their projections to the lateral hypothalamus and regulate phasic events, reflected in accelerated electroencephalogram theta oscillations and increased eye movement density during REM sleep. Calcium imaging reveals that the majority of lateral hypothalamus-projecting mPFC neurons are maximally activated during REM sleep and a subpopulation is recruited during phasic theta accelerations. Our results delineate a cortico-hypothalamic circuit for the top-down control of REM sleep and identify a critical role of the mPFC in regulating phasic events during REM sleep. Hong et al. show that activation of the medial prefrontal cortex induces REM sleep via its projections to the lateral hypothalamus, thus demonstrating a critical role of the cortex in the regulation of REM sleep.

Automated summary

This study reveals the important role of the medial prefrontal cortex (mPFC) in promoting REM sleep through its projections to the lateral hypothalamus. It demonstrates that cortical neurons can trigger REM sleep and regulate phasic events during this sleep stage.