生物
加巴能
辅活化剂
线粒体生物发生
神经科学
转基因
表型
线粒体
细胞生物学
遗传学
基因
转录因子
抑制性突触后电位
作者
Jia Wang,Yun Qi,Jinjun Qian,Hua-Rong Song,Lei Wang,Samuel Eguasi Inkabi,Rujing Xu,Yanmei Hu,Weining Zhang,Haim Einat
出处
期刊:Neuropsychobiology
日期:2019-01-01
卷期号:78 (4): 182-188
被引量:8
摘要
Significant evidence from various sources suggests that structural alterations in mitochondrial function may play a role in both the pathogenesis of mood disorders and the therapeutic effects of available treatments. PGC-1α is a distinct transcriptional regulator designed to mediate the synchronous release of neurotransmitter in the brain and thereby to coordinate a number of gene expression pathways to promote mitochondrial biogenesis and oxidative phosphorylation. The role of PGC-1α in the context of affective disorder phenotypes and treatments has been suggested but not studied in depth. To further investigate the possible involvement of PGC-1α in affective disorders, we generated conditional PGC-1α null mice through transgenic expression of cre recombinase under the control of a Dlx5/6 promoter; cre-mediated excision events were limited to γ-amino-butyric-acid (GABA)-ergic specific neurons. We tested these mice in a battery of behavioral tests related to affective change including spontaneous activity, elevated plus maze, forced swim test, and tail suspension test. Results demonstrated that mice lacking PGC-1α in GABAergic neurons exhibited increased activity across tests that might be related to a mania-like phenotype. These results suggest possible relevance of PGC-1α to affective change, which corresponds with data connecting mitochondrial function and affective disorders and their treatment.
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