Electroconvulsive seizures regulates the Brd1 gene in the frontal cortex and hippocampus of the adult rat

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• 作者：Tue Fryland^a ; ^{tue@humgen.au.dk} ; Betina Elfving^b ; Jane H. Christensen^a ; Ole Mors^b ; Gregers Wegener^b ; ^c ; Anders D. Bø ; rglum^a ; ^b
• 关键词：Electroconvulsive therapy ; BRD1 gene ; Histone acetyltransferase ; Depression ; Schizophrenia ; Bipolar disorder
• 刊名：Neuroscience Letters
• 出版年：2012
• 期刊代码：52_03043940
• 类别：neu
• 出版时间：10 May, 2012
• 卷：516
• 期：1
• 页码：110-113
• 文件大小：289 K

摘要

Depressive disorders represent a significant health concern as they are associated with high social and physical dysfunction and increased risk for suicide. Electroconvulsive therapy (ECT) is the most effective treatment for patients with drug-resistant severe depressive disorders. However, the underlying biological mechanisms of ECT are not well characterized. In particular, the regulation of transcription factors upon ECT has only just started to be unveiled. The schizophrenia and bipolar disorder associated bromodomain containing 1 (BRD1) gene is important for the acetylation of histone H3K14 and holds a key role in normal embryonic development and survival. In this study, we have measured Brd1 mRNA in the hippocampus and the frontal cortex of male Sprague-Dawley rats upon acute and repeated electroconvulsive seizures (ECS) over a period of 10 days. We found an increase in the general expression of Brd1 mRNA in the hippocampus after repeated ECS compared to sham (F = 8.108, P = 0.003). Furthermore, we provide evidence suggesting a decrease in the expression of the Brd1 mRNA variant comprising an extended version of exon 7 (Brd1-L) in the frontal cortex after repeated ECS compared to sham (F = 6.225, P = 0.023). These findings indicate that regulation of the Brd1 gene is part of the biological response to ECS and that splice variants are induced differentially in different brain regions.