Background: Beta-catenin was discovered as a cytoskeletal protein, constituting a link between the cadherins to the actin cytoskeleton. Aside from this function, β-catenin is a key effector molecule in the Wnt signaling pathway, serving as a downstream transcription factor. Methods: In this study, we examined the influence of electroconvulsive seizures (ECS) on the expression of β-catenin, as well as expression of Wnt-2, in rat hippocampus. Repeated administration of generalized seizures increased levels of β-catenin immunoreactivity in the subgranular zone of the hippocampus. To assess the relationship of β-catenin to cell division in the dentate gyrus of the adult rat hippocampus, colocalization of β-catenin with a marker of cell division was examined. Results: Beta-catenin immunoreactivity was consistently localized in newborn cells in this region, indicating a possible role in cell division and differentiation in adult hippocampus. We also found that ECS treatment significantly increased levels of Wnt-2, one of the ligands that activates β-catenin signaling. Conclusions: These results demonstrate that ECS increases Wnt-β-catenin signaling and suggest that this pathway could mediate in part the neuronal adaptations underlying the therapeutic action of this treatment paradigm.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Nov 15 2003|
- Wnt signaling
ASJC Scopus subject areas
- Biological Psychiatry