GABAergic promoter hypermethylation as a model to study the neurochemistry of schizophrenia vulnerability

被引：40

作者：

Costa, Erminio ^{[1
]}

Chen, Ying ^{[2
]}

Dong, Erbo ^{[2
]}

Grayson, Dennis R. ^{[2
]}

Kundakovic, Marija ^{[2
]}

Maloku, Ekrem ^{[2
]}

Ruzicka, William ^{[2
]}

Satta, Rosalba ^{[2
]}

Veldic, Mann ^{[2
]}

Zhubi, Adrian ^{[2
]}

Guidotti, Alessandro ^{[1
]}

机构：

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

[2] Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA

来源：

EXPERT REVIEW OF NEUROTHERAPEUTICS | 2009年 / 9卷 / 01期

关键词：

antipsychotic; chromatin remodeling; DNA demethylase; DNA methyltransferase inhibitor; GABAergic neurotransmission; GAD(67); histone deacetylase inhibitor; psychosis; reelin; valproate; HUMAN REELIN GENE; DNA METHYLTRANSFERASE; BIPOLAR DISORDER; DENDRITIC SPINE; DOWN-REGULATION; MATERNAL-CARE; MOUSE MODEL; ACID; METHYLATION; EXPRESSION;

D O I：

10.1586/14737175.9.1.87

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The neuronal GABAergic mechanisms that mediate the symptomatic beneficial effects elicited by a combination of antipsychotics with valproate (a histone deacetylase inhibitor) in the treatment of psychosis (expressed by schizophrenia or bipolar disorder patients) are unknown. This prompted us to investigate whether the beneficial action of this combination results from a modification of histone tail covalent esterification or is secondary to specific chromatin remodeling. The results suggest that clozapine, or sulpiride associated with valproate, by increasing DNA demethylation with an unknown mechanism, causes a chromatin remodeling that brings about a beneficial change in the epigenetic GABAergic dysfunction typical of schizophrenia and bipolar disorder patients.

引用

页码：87 / 98

页数：12

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