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Expression analysis in a rat psychosis model identifies novel candidate genes validated in a large case-control

A Ingason1, I Giegling1, A M Hartmann1

  • 1Department of Psychiatry, University of Halle-Wittenberg, Halle, Germany.

Translational Psychiatry
|October 14, 2015
PubMed

Insights

This study models NMDA receptor hypofunction in rats, identifying four genes (SF3B1, FOXP1, DLG2, VGLL4) associated with schizophrenia. These findings link NMDA receptor function to schizophrenia genetics and neurodevelopmental disorders.

Area of Science:

  • Neuroscience
  • Genetics
  • Psychiatry

Background:

  • N-methyl-D-aspartate (NMDA)-type glutamate receptor antagonists can induce psychosis and worsen schizophrenia symptoms.
  • NMDA receptor hypofunction is a proposed mechanism underlying schizophrenia pathophysiology.

Purpose of the Study:

  • To develop an animal model of NMDA receptor hypofunction.
  • To identify genes associated with schizophrenia through this model.
  • To investigate the genetic links between NMDA receptor function and schizophrenia.

Main Methods:

  • Chronic administration of low-dose MK-801 to rats to induce NMDA receptor hypofunction.
  • Gene expression profiling in the brains of treated and untreated rats.
  • Genome-wide association study (GWAS) analysis of human orthologs of identified genes in a large schizophrenia cohort.

Main Results:

  • Identified 20 genes with altered expression in the NMDA receptor hypofunction rat model.
  • Found significant association for four human orthologs (SF3B1, FOXP1, DLG2, VGLL4) with schizophrenia in GWAS.
  • Noted that FOXP1, SF3B1, and DLG2 have prior links to neurodevelopmental disorders.

Conclusions:

  • The NMDA receptor hypofunction model successfully identified candidate genes relevant to schizophrenia.
  • SF3B1, FOXP1, DLG2, and VGLL4 represent potential genetic factors contributing to schizophrenia risk.
  • The overlap with neurodevelopmental disorder genes suggests shared biological pathways in psychiatric disorders.

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