Journal article

Molecular mechanisms in mood regulation involving the circadian clock

  • Albrecht, Urs Department of Biology, Unit of Biochemistry, University of Fribourg, Switzerland
    2017
Published in:
  • Frontiers in Neurology. - 2017, vol. 8, p. 30
English The circadian system coordinates activities and functions in cells and tissues in order to optimize body functions in anticipation to daily changes in the environment. Disruption of the circadian system, due to irregular lifestyle such as rotating shift work, frequent travel across time-zones, or chronic stress, is correlated with several diseases such as obesity, cancer, and neurological disorders. Molecular mechanisms linking the circadian clock with neurological functions have been uncovered suggesting that disruption of the clock may be critically involved in the development of mood disorders. In this mini-review, I will summarize molecular mechanisms in which clock components play a central role for mood regulation. Such mechanisms have been identified in the monoaminergic system, the HPA axis, and neurogenesis.A plethora of human genetic studies have identified polymorphisms in clock genes that associate with psychiatric disorders [reviewed in Ref. (1)]. This suggested that abnormalities in clock genes may be one of the causes for the development of mood disorders. At the cellular level, clock genes (Bmal1, Clock, Per, Cry, Rev-erb, and Ror) make up an autoregulatory transcriptional/translational feedback loop with a period of about 24 h (Figure 1, top gray circle) [reviewed in Ref. (2)]. These clock genes and their proteins not only self-promote their own temporally fluctuating transcription but they also regulate transcription of target genes (Figure 1) and/or modulate key molecular pathways via protein–protein interactions, such as the monoaminergic system, the HPA axis, or neurogenic pathways.
Faculty
Faculté des sciences et de médecine
Department
Département de Biologie
Language
  • English
Classification
Biological sciences
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/305320
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