Journal
NEUROPSYCHOBIOLOGY
Volume 78, Issue 4, Pages 182-188Publisher
KARGER
DOI: 10.1159/000500738
Keywords
Bipolar disorder; Mania; Animal model; Mitochondria
Categories
Funding
- Clinic Development Fund of Jiangsu [BE2016724, BL2014068, SH2015070]
- Science and Technology Department Fund of Jiangsu Province [H201549, LGY2017025]
- Universities Natural Science Fund of Jiangsu [16KJB180005]
- Natural Science Foundation of China [81671053]
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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-1 alpha 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-1 alpha 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-1 alpha in affective disorders, we generated conditional PGC-1 alpha null mice through transgenic expression of cre recombinase under the control of a Dlx5/6 promoter; cre-mediated excision events were limited to gamma-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-1 alpha in GABAergic neurons exhibited increased activity across tests that might be related to a mania-like phenotype. These results suggest possible relevance of PGC-1 alpha to affective change, which corresponds with data connecting mitochondrial function and affective disorders and their treatment.
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