Phosducin-like protein levels in leukocytes of patients with major depression and in rat cortex: The effect of chronic treatment with antidepressants

Angela Matuzany-Ruban, Gabriel Schreiber, Peter Farkash, Sofia Avissar

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

The importance of signal transduction processes beyond receptors involving receptor-G protein coupling, in both the pathophysiology and the treatment of mood disorders, is well documented. Thus, regulatory elements of G protein function may play a role in the molecular mechanisms underlying these alterations. Phosducin-like proteins, a family of regulators of G protein function expressed throughout brain and body, modulate G protein function by high affinity sequestration of G protein-βγ subunits, thus impeding G protein-mediated signal transmission by both Gα and Gβγ subunits. An important consequence of Gβγ neutralization is the prevention of G protein-coupled receptor kinase phosphorylation resulting in a temporary protection to agonist-bound receptor desensitization. Phosducin-like protein levels were measured in brain cortices of rats chronically treated with one of five classes of antidepressants: imipramine, venlafaxine, maprotiline, citalopram, and moclobemide. None of the antidepressant treatments had any significant effect on phosducin-like protein levels. Phosducin-like protein levels were evaluated in mononuclear leukocytes from a group of 15 patients diagnosed with major depressive episode, both before the initiation of antidepressant treatment and after 4 weeks of antidepressant medication. No protein changes were found in leukocytes of either untreated patients with major depressive disorder or after 4 weeks of the treatment in comparison with healthy volunteers.

Original languageEnglish
Pages (from-to)287-294
Number of pages8
JournalPsychiatry Research
Volume141
Issue number3
DOIs
StatePublished - 30 Mar 2006

Keywords

  • G protein regulation
  • Gβγ subunits sequestration
  • Monoamine reuptake inhibitor
  • Signal transduction
  • Unipolar depression

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