Association study of polymorphisms in the GluR5 kainate receptor gene (GRIK1) with schizophrenia

Hiroki Shibata, Akiko Joo, Yo Fujii, Ayako Tani, Chieko Makino, Naotsugu Hirata, Rumiko Kikuta, Hideaki Ninomiya, Nobutada Tashiro, Yasuyuki Fukumaki

Research output: Contribution to journalArticlepeer-review

33 Citations (Scopus)


The glutamatergic dysfunction hypothesis suggests genes involved in glutamatergic transmission as candidates for schizophrenia susceptibility genes. We screened single nucleotide polymorphisms (SNPs) in the entire coding sequence of the GluR5 kainate receptor gene, GRIK1, by polymerase chain reaction-single strand conformation polymorphism and direct sequencing. We identified six SNPs including three known ones, 522A/C (174T, synonymous), 1173C/T (391D, synonymous), and 2705C/T (902L/S), as well as three novel ones, 995C/T (332A/V), 2400C/T (800L, synonymous), and 2585A/G (862R/Q). We genotyped Japanese samples of schizophrenia (n = 193-203) and healthy controls (n = 199-215) for three SNPs those were commonly observed in our samples, 522A/C, 1173C/T, and 2705C/T. We observed no significant associations of the SNPs and their haplotypes with schizophrenia. Therefore, we conclude that GRIK1 does not play a major role in schizophrenia pathogenesis in the Japanese population.

Original languageEnglish
Pages (from-to)139-144
Number of pages6
JournalPsychiatric Genetics
Issue number3
Publication statusPublished - 2001

All Science Journal Classification (ASJC) codes

  • Genetics
  • Genetics(clinical)
  • Psychiatry and Mental health
  • Biological Psychiatry


Dive into the research topics of 'Association study of polymorphisms in the GluR5 kainate receptor gene (GRIK1) with schizophrenia'. Together they form a unique fingerprint.

Cite this