期刊
JOURNAL OF PSYCHOPHARMACOLOGY
卷 25, 期 1, 页码 87-96出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/0269881110367724
关键词
Anxiety; benzodiazepine; GABA(A) receptor; prodynorphin gene
资金
- Red Tematica de Investigacion Cooperativa en Salud (RETICS, Instituto de Salud Carlos III, MICINN and FEDER, Madrid, Spain) [RD06/0001/1004]
- MSC [FIS 05/0429]
- FEDER [FIS 05/0429]
This study evaluated the role of prodynorphin gene in the regulation of anxiety and associated molecular mechanisms. Emotional responses were assessed using the light-dark test, elevated plus maze and social interaction tests in prodynorphin knockout and wild-type mice. Corticotrophin releasing factor and proopiomelanocortin gene expressions in the hypothalamus were evaluated after restraint stress using in situ hybridization. The anxiolytic efficacy of bromazepam and GABA(A) receptor subunits gene expression in the amygdala were also assessed in both genotypes. The deletion of prodynorphin increased anxiety-like behaviours and proopiomelanocortin gene expression in the arcuate nucleus (two-fold). Moreover, the anxiolytic action of bromazepam was significantly attenuated in the mutant mice. Decreased GABA(A)gamma(2) and increased GABA(A)beta(2) gene expression receptor subunits were found in the amygdala of prodynorphin knockout mice. These results indicate that deletion of prodynorphin gene is associated with increased anxiety-like behaviours, enhanced sensibility response to stress stimuli, reduced anxiolytic efficacy of bromazepam and altered expression of the GABA(A) receptor subunits.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据