Association between the ionotropic glutamate receptor kainate 3 (GRIK3) ser310ala polymorphism and schizophrenia

S. Begni, M. Popoli, S. Moraschi, S. Bignotti, G. B. Tura, M. Gennarelli

Research output: Contribution to journalArticlepeer-review


Schizophrenia is a severe psychiatric illness characterised by disturbance of thought, hallucination and delusions.1 Several studies have suggested that dysfunctions in the glutamatergic transmission are linked to the pathogenesis of schizophrenia, and in particular an excessive activation of glutamate receptors seems to be related to the disruption of neuronal ionic gradients leading to excitotoxicity.2-7 Numerous findings suggested that the kainate ionotropic glutamate receptors are primarily involved in this mechanism. Recently it has been demonstrated that the GRIK3 gene encoding for the ionotropic glutamate receptor kainate 3 contains a functional polymorphism (T928G) leading to the substitution of a serine with an alanine in position 310 of the protein sequence.8-11 We performed an association study between the ser310ala GRIK3 polymorphism and schizophrenia in a sample of 99 schizophrenic patients and 116 controls. We found a significant difference in the genotype distribution and in particular considering the ala allele as dominant (P = 0.0105, odds ratio (OR) 2.031, 95% confidence interval (Cl) 1.177-3.504). This finding suggests a potential role for GRIK3 for susceptibility to schizophrenia.

Original languageEnglish
Pages (from-to)416-418
Number of pages3
JournalMolecular Psychiatry
Issue number4
Publication statusPublished - 2002


  • Association study
  • cSNP
  • Expression
  • Kainate receptor
  • Neuronal plasticity

ASJC Scopus subject areas

  • Molecular Biology
  • Psychiatry and Mental health


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