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

研究成果: Contribution to journalArticle査読

31 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)139-144
ページ数6
ジャーナルPsychiatric Genetics
11
3
DOI
出版ステータス出版済み - 2001

All Science Journal Classification (ASJC) codes

  • 遺伝学
  • 遺伝学(臨床)
  • 精神医学および精神衛生
  • 生物学的精神医学

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