The cannabinoid receptor is a mediator for the hallucinogenic action of morphine, heroine and related drugs. A cannabinoid hypothesis for the pathogenesis of schizophrenia is possible because morphine-like agents induce psychosis in its abusers resembling schizophrenia and its positive symptoms. CNR1 gene encodes the human CB1 receptor, a subclass of cannabinoid receptors. We examined polymorphism 1359G/A of codon 453 in coding region of CNR1 by RFLP analysis using Msp I. Distribution of genotypes, G/G, G/A and A/A type, in normal controls (all are Japanese, N= 106) was 92.5 %, 5.7 % and 1.9 %, respectively. The allele frequencies of G and A alleles were 95.3 % and 4.7 % , respectively. This result was quite different from Caucasians who showed 76% G alleles and 24% A alleles reported by Gadzicki D, et al. (1999). In the comparison of CNR1 gene polymorphism with schizophrenia (N=154), there was no significant difference when analyzed using all schizophrenic patients or using the subcategories of paranoid, hebephrenia and schizoaffective disorders. Although the polymorphism examined was silent, the present study did not support a cannabinoid hypothesis for schizophrenia.
|Number of pages||1|
|Journal||American Journal of Medical Genetics - Neuropsychiatric Genetics|
|Publication status||Published - Aug 7 2000|
ASJC Scopus subject areas
- Psychiatry and Mental health
- Cellular and Molecular Neuroscience