An essential role for mef2c in the cortical response to loss of sleep in mice

Theresa E. Bjorness, Ashwinikumar Kulkarni, Volodymyr Rybalchenko, Ayako Suzuki, Catherine Bridges, Adam J. Harrington, Christopher W. Cowan, Joseph S. Takahashi, Genevieve Konopka, Robert W. Greene

Research output: Contribution to journalArticlepeer-review

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 sleeploss 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. One Sentence Summary: MEF2C is critical to the response to sleep loss.

Original languageEnglish (US)
Pages (from-to)1-46
Number of pages46
JournaleLife
Volume9
DOIs
StatePublished - Aug 2020

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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