Chronic social stress induces mitochondrial DNA mutation and mitochondrial dysfunction in mouse brains

Wednesday, November 06, 2013 — Poster Session I
4:00 p.m. – 6:00 p.m.	FAES Academic Center (Upper-Level Terrace)	NIMH	NEURO-7

Authors

K.Z. Duan
X. Liu
T. Ni
J. Zhu
Z. Li

Abstract

Mitochondrial dysfunction and mutations of mitochondrial DNA (mtDNA) are implicated in psychiatric disorders. However, little is known about the effect of chronic social stress on mitochondria. Here, we used the chronic social defeat (CSD) model, a mouse model of social stress, which induces anxiety, depression and learning abnormalities, to investigate the change in brain mitochondria following social stress. Our analysis of mtDNA mutations revealed that CSD caused a moderate increase in the mutation rate of mtDNA selectively in amygdalae but not in the hippocampus. Moreover, our mitochondrial function analysis showed that mitochondrial membrane potential (assessed by staining with the mitochondrial membrane potential indicator TMRE) and the activity of cytochrome c oxidase (COX) in the amygdale but not in the hippocampus were reduced in mice subject to CSD. The decrease in COX activity is likely due to less COX expression in the CSD mice, as we detected a lower level of COX subunit I by immunoblotting. These results indicate that chronic social defeat stress undermines mitochondrial function and reduces the stability of mtDNA. Hence, mitochondrial dysfunction might contribute to social stress-induced behavioral impairment.