Lack of effect of mood stabilizers or neuroleptics on GSK-3β protein levels and GSK-3 activity

Nitsan Kozlovsky, Carmit Nadri, Robert H. Belmaker, Galila Agam

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Glycogen synthase kinase (GSK)-3β protein levels and GSK-3 activity were previously found to be over 40% reduced in the post-mortem prefrontal cortex of schizophrenic patients. Lithium and valproate have been reported to selectively inhibit GSK-3. We hypothesized that in-vivo administration of lithium and valproate would result in up-regulation of GSK-3β protein levels and GSK-3 activity. The present study aimed to evaluate the possible involvement of neuroleptic treatment in the decrease of GSK-3 in schizophrenia. Rat frontal cortex GSK-3β protein levels and GSK-3 activity were measured following administration of therapeutic doses of lithium or valproate for 11 d, or of haloperidol, chlorpromazine or clozapine for 21 d. None of the drugs induced a change in GSK-3β protein levels. All the drugs except chlorpromazine (which was not tested) did not affect GSK-3 activity. This suggests that GSK-3β inhibition by lithium or valproate does not induce regulation of protein levels or activity and that the reduction in GSK-3β protein levels and GSK-3 activity in the post-mortem prefrontal cortex of schizophrenic patients is not neuroleptic-treatment related.

Original languageEnglish
Pages (from-to)117-120
Number of pages4
JournalInternational Journal of Neuropsychopharmacology
Volume6
Issue number2
DOIs
StatePublished - 1 Jun 2003

Keywords

  • Animal model
  • Frontal cortex
  • GSK-3β
  • Mood stabilizers
  • Neuroleptics

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health
  • Pharmacology (medical)

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