An essential role for MEF2C in the cortical response to loss of sleep in mice

Elife. 2020 Aug 27;9:e58331. doi: 10.7554/eLife.58331.

Abstract

Neuronal activity and gene expression in response to the loss of sleep can provide a window into the enigma of sleep function. Sleep loss is associated with brain differential gene expression, an increase in pyramidal cell mEPSC frequency and amplitude, and a characteristic rebound and resolution of slow wave sleep-slow wave activity (SWS-SWA). However, the molecular mechanism(s) mediating the sleep-loss response are not well understood. We show that sleep-loss regulates MEF2C phosphorylation, a key mechanism regulating MEF2C transcriptional activity, and that MEF2C function in postnatal excitatory forebrain neurons is required for the biological events in response to sleep loss in C57BL/6J mice. These include altered gene expression, the increase and recovery of synaptic strength, and the rebound and resolution of SWS-SWA, which implicate MEF2C as an essential regulator of sleep function.

Keywords: MEF2C; gene expression; mouse; neuroscience; sleep; sleep deprivation; slow wave activity.

Publication types

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

MeSH terms

  • Animals
  • Cerebral Cortex / physiology*
  • Gene Expression Regulation*
  • MEF2 Transcription Factors / genetics
  • MEF2 Transcription Factors / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Phosphorylation
  • Sleep / physiology
  • Sleep Deprivation*
  • Transcription, Genetic

Substances

  • MEF2 Transcription Factors
  • Mef2c protein, mouse

Associated data

  • GEO/GSE144957