1. ¹Department of Psychiatry, Fujita Health University School of Medicine, Aichi, Japan
2. ²Department of Psychiatry, Nagoya City University Medical School, Nagoya, Japan
3. ³Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan
4. ⁴Japanese Genetics Initiative for Drug Abuse (JGIDA), Japan
5. ⁵Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Japan
6. ⁶Department of Psychiatry, Graduate School of Medicine, Chiba University, Chiba, Japan
7. ⁷Department of Neuropsychiatry, Kurume University School of Medicine, Kurume, Japan
8. ⁸Division of Psychiatry, National Center Hospital for Mental, Nervous and Muscular Disorders, National Center of Neurology and Psychiatry, Tokyo, Japan
9. ⁹Division of Psychogeriatrics, National Institute of Mental Health, National Center of Neurology and Psychiatry, Chiba, Japan
10. ¹⁰Department of Neuroscience, Division of Psychobiology, Tohoku University Graduate School of Medicine, Sendai, Japan
11. ¹¹Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan

Correspondence: Dr N Iwata, Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan. Tel: +81 562 93 9250; Fax: +81 562 93 1831; E-mail: nakao@fujita-hu.ac.jp

Received 18 March 2004; Revised 12 October 2004; Accepted 19 October 2004.

Abstract

Psychostimulant use disorder and schizophrenia have a substantial genetic basis. Evidence from human and animal studies on the involvement of the -aminobutyric acid (GABA) system in methamphetamine (METH) use disorder and schizophrenia is mounting. As we tested for the association of the human GABA_A receptor gamma 2 subunit gene (GABRG2) with each diagnostic group, we used a case–control design with a set of 178 subjects with METH use disorder, 288 schizophrenics and 288 controls. First, we screened 96 controls and identified six SNPs in GABRG2, three of whom we newly reported. Next, we selected two SNPs, 315C>T and 1128+99C>A, as representatives of the linkage disequilibrium blocks for further case–control association analysis. Although no associations were found in either allelic or genotypic frequencies, we detected a haplotypic association in GABRG2 with METH use disorder, but not with schizophrenia. This finding partly replicates a recent case–control study of GABRG2 in METH use disorder, and thus indicates that GABRG2 may be one of the susceptibility genes of METH use disorder.