Control of non-REM sleep by ventrolateral medulla glutamatergic neurons projecting to the preoptic area

In this study, Teng et al. identify a population of glutamatergic neurons in the ventrolateral medulla that control Non-Rapid Eye Movement (NREM) sleep in mice. They uncover an excitatory brainstem-hypothalamic circuit that controls wake-sleep transitions. Understanding the neural mechanisms underlying sleep state transitions is a fundamental goal of neurobiology and important for the development of new treatments for insomnia and other sleep disorders. Yet, brain circuits controlling this process remain poorly understood. Here we identify a population of sleep-active glutamatergic neurons in the ventrolateral medulla (VLM) that project to the preoptic area (POA), a prominent sleep-promoting region, in mice. Microendoscopic calcium imaging demonstrate that these VLM glutamatergic neurons display increased activity during the transitions from wakefulness to Non-Rapid Eye Movement (NREM) sleep. Chemogenetic silencing of POA-projecting VLM neurons suppresses NREM sleep, whereas chemogenetic activation of these neurons promotes NREM sleep. Moreover, we show that optogenetic activation of VLM glutamatergic neurons or their projections in the POA initiates NREM sleep in awake mice. Together, our findings uncover an excitatory brainstem-hypothalamic circuit that controls the wake-sleep transitions.

Automated summary

This study identifies a population of glutamatergic neurons that control sleep state transitions in mice and uncovers an excitatory brainstem-hypothalamic circuit involved in these transitions.