Mecanismos moleculares relacionados con la vía WNT / B-catenina y la enfermedad psiquiátrica

Resumo

Current antidepressant drugs raise the level of monoamines in the synapse, but their clinical efficacy is delayed several weeks. This justifies the need to develop new faster, safer and effective antidepressants. Our objective is to identify molecular mediators of plasticity / neurogenesis as targets for the development of fast-acting antidepressants knowing that: agonists of 5-HT4 receptors induce a rapid antidepressant effects in animals also the Wnt signaling pathway Wnt -ß-catenin promotes changes in neuroplasticity by classic antidepressants and 5HT4 agonists. We observed slight increases in the expression level of selected genes with SSRIs. Venlafaxine increases more and early gene expression of Wnt / ß-catenin, RS67333 increase less and later the expression of genes involved in the Wnt / ß-catenin, but increases earliest and greater gene expression pathways involved Ccnd1 and Notch.