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Abnormal retinoid and TrkB signaling in the prefrontal cortex in mood disorders

Xin-Rui Qi1, Jun Zhao2, Ji Liu2

  • 1CAS Key Laboratory of Brain Function and Diseases, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230026, PR China Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam 1105BA, The Netherlands.

Cerebral Cortex (New York, N.Y. : 1991)
|August 21, 2013
PubMed

Insights

Mood disorders like depression involve reduced retinoid signaling and brain-derived neurotrophic factor (BDNF) in the prefrontal cortex. Targeting retinoid pathways may offer novel antidepressant treatments by activating TrkB expression.

Area of Science:

  • Neuroscience
  • Molecular Psychiatry
  • Neurobiology of Mood Disorders

Background:

  • Mood disorders are associated with prefrontal cortex alterations.
  • Retinoid signaling, BDNF, and TrkB are implicated in depression.
  • Reduced expression of these pathways is observed in depressed individuals.

Purpose of the Study:

  • To investigate the role of retinoid signaling and BDNF-TrkB pathway in the prefrontal cortex of depressed patients.
  • To explore the interaction between retinoic acid receptor-alpha (RARα) and TrkB.
  • To identify potential novel antidepressant treatment targets.

Main Methods:

  • Analysis of postmortem prefrontal cortex/anterior cingulate cortex (ACC) from elderly depressed patients and control subjects.
  • Assessment of mRNA levels for retinoid signaling elements, BDNF, and TrkB.
  • Utilizing a rat model of chronic unpredictable mild stress.
  • In vitro studies to examine RARα's effect on the TrkB promoter.

Main Results:

  • Significantly reduced mRNA levels of retinoid signaling components, BDNF, and TrkB isoforms in depressed patients' ACC.
  • Similar alterations observed in rats under chronic stress.
  • RARα can bind to and activate the TrkB promoter, suggesting a direct interaction.

Conclusions:

  • Retinoid and BDNF-TrkB signaling are compromised in the prefrontal cortex in mood disorders.
  • Transcriptional upregulation of TrkB by RARα presents a mechanism for their interaction.
  • The retinoid signaling pathway offers a potential novel target for antidepressant therapies.
Keywords:
anterior cingulate cortexbrain-derived neurotrophic factordorsolateral prefrontal cortexmood disorderretinoic acid receptor-α

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