An Inhibitory Lateral Hypothalamic-Preoptic Circuit Mediates Rapid Arousals from Sleep

Curr Biol. 2019 Dec 16;29(24):4155-4168.e5. doi: 10.1016/j.cub.2019.10.026. Epub 2019 Nov 21.

Abstract

Among the neuronal populations implicated in sleep-wake control, the ventrolateral preoptic (VLPO) nucleus has emerged as a key sleep-promoting center. However, the synaptic drives that regulate the VLPO to control arousal levels in vivo have not to date been identified. Here, we show that sleep-promoting galaninergic neurons within the VLPO nucleus, defined pharmacologically and by single-cell transcript analysis, are postsynaptic targets of lateral hypothalamic GABAergic (LHGABA) neurons and that activation of this pathway in vivo rapidly drives wakefulness. Ca2+ imaging from LHGABA neurons indicate that they are both wake and rapid eye movement (REM)-sleep active. Consistent with the potent arousal-promoting property of the LHGABA → VLPO pathway, presynaptic inputs to LHGABA neurons originate from several canonical stress- and arousal-related network nodes. This work represents the first demonstration that direct synaptic inhibition of the VLPO area can suppress sleep-promoting neurons to rapidly promote arousal.

Keywords: AAV; CRACM; EEG; GABA; VLPO; fiber photometry; galanin; insomnia; optogenetics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arousal / physiology
  • Brain / physiology
  • Electroencephalography / methods
  • Female
  • GABAergic Neurons / metabolism
  • Hypothalamic Area, Lateral / physiology
  • Hypothalamus / physiology
  • Male
  • Mice
  • Neurons / physiology
  • Preoptic Area / metabolism*
  • Preoptic Area / physiology
  • Sleep / physiology*
  • Sleep Disorders, Circadian Rhythm / physiopathology
  • Wakefulness / physiology*