Characterization of the action of antipsychotic subtypes on valproate-induced chromatin remodeling

被引：91

作者：

Guidotti, Alessandro ^{[1
]}

Dong, Erbo ^{[1
]}

Kundakovic, Marija ^{[1
]}

Satta, Rosalba ^{[1
]}

Grayson, Dennis R. ^{[1
]}

Costa, Erminio ^{[1
]}

机构：

[1] Univ Illinois, Dept Psychiat, Inst Psychiat, Chicago, IL 60612 USA

来源：

TRENDS IN PHARMACOLOGICAL SCIENCES | 2009年 / 30卷 / 02期

关键词：

GLUTAMIC-ACID DECARBOXYLASE; PREFRONTAL CORTEX; BIPOLAR DISORDER; DNA-METHYLATION; REELIN GENE; GABAERGIC INTERNEURONS; SCHIZOPHRENIA; NEURONS; DEMETHYLATION; DYSFUNCTION;

D O I：

10.1016/j.tips.2008.10.010

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Recent advances in schizophrenia (SZ) research indicate that the telencephalic gamma-aminobutyric acid (GABA)ergic neurotransmission deficit associated with this psychiatric disorder probably is mediated by the hypermethylation of the glutamic acid decarboxylase 67 (GAD(67)), reelin and other GABAergic promoters. A pharmacological strategy to reduce the hypermethylation of GABAergic promoters is to induce a DNA-cytosine demethylation by altering the chromatin remodeling with valproate (VPA). When co-administered with VPA, the clinical efficacy of atypical antipsychotics is enhanced. This prompted us to investigate whether this increase in drug efficacy is related to a modification of GABAergic-promoter methylation via chromatin remodeling. Our previous and present results strongly indicate that VPA facilitates chromatin remodeling when it is associated with clozapine or sulpiride but not with haloperidol or olanzapine. This remodeling might contribute to reelin- and GAD(67)-promoter demethylation and might reverse the GABAergic-gene-expression downregulation associated with SZ morbidity.

引用

页码：55 / 60

页数：6

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