AI Article Synopsis
- ACTH-treated rats are used as a model for studying depression that doesn't respond to tricyclic antidepressants.
- Treatment with ACTH lowered the number of new brain cells in the hippocampus and reduced brain-derived neurotrophic factor (BDNF) levels, both crucial for neurogenesis.
- Combining imipramine, lithium, and electroconvulsive treatment helped reverse these effects, indicating a potential pathway to address antidepressant-resistant depression through enhanced neurogenesis.
Article Abstract
We previously reported that adrenocorticotropic hormone (ACTH)-treated rats serve as a valuable animal model for tricyclic antidepressant-resistant depressive conditions. The present study was undertaken to investigate the changes in neurogenesis in the hippocampus of ACTH-treated rats. Chronic treatment of ACTH decreased the number of bromodeoxyuridine-labeled cells in the dentate gyrus, and the coadministration of imipramine and lithium, and electroconvulsive stimuli recovered these reductions. Furthermore, chronic ACTH treatment also decreased the expression of brain-derived neurotrophic factor, and the coadministration of imipramine and lithium, and electroconvulsive stimuli recovered these reductions. These results suggest that antidepressant-resistant depression is caused by the suppression of neurogenesis, and the coadministration of imipramine and lithium, and electroconvulsive stimuli exert an antidepressant-like effect by recovering proliferative signals and neurogenesis.
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| http://dx.doi.org/10.1248/yakushi.132.173 | DOI Listing |
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