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Neuropsychobiology. 2019 Jul 2:1-7. doi: 10.1159/000500738. [Epub ahead of print]

Mice Lacking the Transcriptional Coactivator PGC-1α Exhibit Hyperactivity.

Author information

1
Department of Neurology, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
2
School of Medicine, Jiangsu University, Zhenjiang, China.
3
Mental Health Center, Zhenjiang, China.
4
School of Behavioral Sciences, Tel Aviv-Yaffo Academic College, Tel-Aviv, Israel, haimh@mta.ac.il.

Abstract

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.

KEYWORDS:

Animal model; Bipolar disorder; Mania; Mitochondria

PMID:
31266022
DOI:
10.1159/000500738

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