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Circadian Rhythms and Gene Regulation02:19

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The biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent years,...
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Parallel Measurement of Circadian Clock Gene Expression and Hormone Secretion in Human Primary Cell Cultures
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Cellular circadian clocks in mood disorders.

Michael J McCarthy1, David K Welsh

  • 1Department of Psychiatry, Veterans Affairs San Diego Healthcare System, San Diego, CA, USA.

Journal of Biological Rhythms
|September 27, 2012
PubMed
Summary
This summary is machine-generated.

Circadian clock dysfunction in non-suprachiasmatic nucleus (SCN) brain regions may underlie mood disorders like bipolar disorder (BD) and major depressive disorder (MDD). Studying cellular clocks in accessible tissues offers a new way to test this hypothesis.

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10:38

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Published on: September 27, 2012

Area of Science:

  • Neuroscience
  • Chronobiology
  • Psychiatry

Background:

  • Bipolar disorder (BD) and major depressive disorder (MDD) are heritable conditions linked to disrupted circadian rhythms.
  • The role of circadian clock dysfunction in these mood disorders is controversial and difficult to test.
  • Cellular circadian clocks exist beyond the suprachiasmatic nucleus (SCN), in areas like the lateral habenula, ventral tegmentum, and hippocampus, which are involved in mood regulation.

Purpose of the Study:

  • To test the hypothesis that circadian clock dysfunction in non-SCN brain regions is a trait marker for mood disorders.
  • To investigate the potential role of pathological genetic variants in non-SCN clock dysfunction.
  • To explore novel methods for assessing cellular clock function in mood disorders.

Main Methods:

  • Examining SCN-dependent rhythms (body temperature, melatonin) in BD and MDD patients, noting their limitations as indirect indicators.
  • Proposing the use of reporters of rhythmic clock gene expression in peripheral cells or from mouse models as a direct assay.
  • Leveraging modern chronobiology tools and insights to study cellular clocks.

Main Results:

  • Previous studies on SCN outputs may have missed genetic defects affecting non-SCN clocks due to the SCN's resistance to perturbation.
  • Non-SCN cellular clocks, including those in peripheral tissues, may be more representative of mood-regulating neurons in patients.
  • Direct assays of clock gene expression in cellular clocks offer a promising approach.

Conclusions:

  • Circadian clock dysfunction in non-SCN cellular clocks is a plausible, testable hypothesis for the pathophysiology of BD and MDD.
  • Studying peripheral cellular clocks provides a more direct and accessible method to assess clock function in mood disorders.
  • This research direction could definitively test the role of cellular circadian clocks in the development and progression of mood disorders.