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Polygraphic Recording Procedure for Measuring Sleep in Mice
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Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.

Jennifer A Mohawk1,2, Kimberly H Cox1, Makito Sato2,3

  • 1Department of Neuroscience, Peter O'Donnell Jr. Brain Insitute.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|August 18, 2019
PubMed
Summary

Myocyte enhancer factor-2 D (MEF2D) is crucial for regulating circadian rhythms and sleep patterns in male mice. This transcription factor influences the suprachiasmatic nucleus (SCN) output, impacting behavior without altering the internal SCN clock.

Keywords:
MEF2Dcircadiansleep

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Area of Science:

  • Neuroscience
  • Chronobiology
  • Molecular Biology

Background:

  • Myocyte enhancer factor-2 (MEF2) transcription factors are vital for circadian behavior in fruit flies.
  • The role of MEF2 in mammalian circadian systems, particularly in the brain, remains largely uncharacterized.
  • MEF2D is notably expressed in the suprachiasmatic nucleus (SCN), the master circadian clock in the hypothalamus.

Purpose of the Study:

  • To investigate the function of MEF2D in the mammalian circadian system.
  • To determine MEF2D's role in regulating locomotor activity, sleep patterns, and the SCN's circadian output.
  • To elucidate the impact of MEF2D on the central circadian clock and related behaviors.

Main Methods:

  • Utilized conventional and brain-specific Mef2d knockout (Mef2d-/-) mouse models.
  • Assessed circadian free-running period of locomotor activity and sleep patterns in Mef2d-/- mice.
  • Crossed Mef2d-/- mice with Per2::luc reporter mice to evaluate the SCN's endogenous circadian period.

Main Results:

  • MEF2D deficiency in mice disrupted the circadian free-running period of locomotor activity.
  • Mef2d knockout mice exhibited abnormal sleep patterns.
  • These behavioral alterations occurred independently of changes to the SCN's intrinsic circadian period, as shown by Per2::luc reporter assays.
  • Findings suggest MEF2D affects SCN output rather than the SCN's timekeeping mechanism.

Conclusions:

  • MEF2D is essential for maintaining normal circadian rhythms and sleep in male mice.
  • MEF2D's influence on circadian behavior appears to be mediated through SCN output pathways, not central clock function.
  • These findings highlight a novel role for MEF2 proteins in the central nervous system and circadian regulation, with implications for understanding jet lag and shift work-related disorders.