Expression of monoamine transporters, nitric oxide synthase 3, and neurotrophin genes in antidepressant-stimulated astrocytes

  • Sarah Kittel-Schneider
  • , Gunter Kenis
  • , Julia Schek
  • , Daniel van den Hove
  • , Jos Prickaerts
  • , Klaus Peter Lesch
  • , Harry Steinbusch
  • , Andreas Reif

Research output: Contribution to journalArticlepeer-review

Abstract

Background: There is increasing evidence that glial cells play a role in the pathomechanisms of mood disorders and the mode of action of antidepressant drugs. Methods: To examine whether there is a direct effect on the expression of different genes encoding proteins that have been implicated in the pathophysiology of affective disorders, primary astrocyte cell cultures from rats were treated with two different antidepressant drugs, imipramine and escitalopram, and the RNA expression of brain-derived neurotrophic factor (Bdnf), serotonin transporter (5Htt), dopamine transporter (Dat), and endothelial nitric oxide synthase (Nos3) was examined. Results: Stimulation of astroglial cell culture with imipramine, a tricyclic antidepressant, led to a significant increase of the Bdnf RNA level whereas treatment with escitalopram did not. In contrast, 5Htt was not differentially expressed after antidepressant treatment. Finally, neither Dat nor Nos3 RNA expression was detected in cultured astrocytes. Conclusion:These data provide further evidence fora role of astroglial cells in the molecular mechanisms of action of antidepressants.

Original languageEnglish
Article numberArticle 33
JournalFrontiers in Psychiatry
Volume3
Issue numberAPR
DOIs
Publication statusPublished - 2012
Externally publishedYes

Keywords

  • Antidepressant
  • Astrocytes
  • BDNF
  • Depression
  • Gene expression
  • Glia
  • Mechanism of action
  • Nitric oxide synthase

Fingerprint

Dive into the research topics of 'Expression of monoamine transporters, nitric oxide synthase 3, and neurotrophin genes in antidepressant-stimulated astrocytes'. Together they form a unique fingerprint.

Cite this