| First Author | Wang J | Year | 2019 |
| Journal | Neuropsychobiology | Volume | 78 |
| Issue | 4 | Pages | 182-188 |
| PubMed ID | 31266022 | Mgi Jnum | J:294247 |
| Mgi Id | MGI:6455131 | Doi | 10.1159/000500738 |
| Citation | Wang J, et al. (2019) Mice Lacking the Transcriptional Coactivator PGC-1alpha Exhibit Hyperactivity. Neuropsychobiology 78(4):182-188 |
| abstractText | 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-1alpha 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-1alpha 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-1alpha in affective disorders, we generated conditional PGC-1alpha 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-1alpha in GABAergic neurons exhibited increased activity across tests that might be related to a mania-like phenotype. These results suggest possible relevance of PGC-1alpha to affective change, which corresponds with data connecting mitochondrial function and affective disorders and their treatment. |
