Chronic electroconvulsive seizure up-regulates β-catenin expression in rat hippocampus: role in adult neurogenesis

Abstract

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.