| Literature DB >> 12799619 |
Mitsuyuki Matsumoto1, Cynthia Shannon Weickert, Senda Beltaifa, Bhaskar Kolachana, Jingshan Chen, Thomas M Hyde, Mary M Herman, Daniel R Weinberger, Joel E Kleinman.
Abstract
Human prefrontal cortical neurons express catechol O-methyltransferase (COMT), an enzyme that inactivates the neurotransmitter dopamine. A functional polymorphism of COMT, Val(108/158) Met, affects prefrontal function, and the high-activity Val allele has been reported to be a genetic risk factor for schizophrenia. We used in situ hybridization histochemistry to measure mRNA levels of COMT in the dorsolateral prefrontal cortex (DLPFC) of patients with schizophrenia (N=14) and of normal controls (N=15). While the groups did not differ in terms of mean level of COMT mRNA, there was a significantly different laminar pattern of COMT mRNA expression in pyramidal neurons (F=2.68, df=4,108, P <0.04); patients with schizophrenia had relatively lower levels in the superficial (II/III) layers and higher levels in the intermediate/deep (IV/V) layers (P&<0.01), while in controls, the expression was homogeneous across layers. Neither the mean level nor the laminar distribution of COMT mRNA was related to the Val(108/158) Met genotype, suggesting that the feedback regulation of mRNA level is not a compensation for the functional effect of the COMT polymorphism. The disease-related laminar difference of COMT expression may be involved in dysregulation of dopamine signaling circuits in the DLPFC of patients with schizophrenia.Entities:
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Year: 2003 PMID: 12799619 DOI: 10.1038/sj.npp.1300218
Source DB: PubMed Journal: Neuropsychopharmacology ISSN: 0893-133X Impact factor: 7.853