Behavioral and neurogenetic opposite changes depending on β-catenin expression
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AuthorAlonso Bustamante, María
The regulatory effect of β-catenin (a key mediator in the Wnt signaling pathway) upon neuronal differentiation/proliferation is proposed to be contributing to mood disorders pathophysiology within the context of neurogenesis and neuroplasticity in these diseases (Pilar-Cuéllar et al., 2013). Additionally, antidepressants may, at least in part, exert their neurogenic effects in the subgranular zone of the hippocampus by increasing levels of β-catenin (Mostany et al., 2008). A study with post-mortem prefrontal cortex observed a deregulation of Wnt/GSK3β signalling associated with a lifetime of depression, showing that β-catenin protein levels were decreased in the vPFC of depressed subject (Karege et al., 2012). To further understand the role of β-catenin in depression/anxiety, we generated conditional mice either lacking (KO) or overexpressing (OE) β-catenin in progenitor cells of the subgranular zone (SGZ) of the hippocampus. Both transgenic lines express CreERT under the control of the astrocyte-specific glutamate transporter (GLAST) promoter inducible by tamoxifen administration (Mori et al., 2006). Here we show that altered levels of β-catenin in progenitor cells of hippocampus modulate hippocampal neurogenesis by measuring Ki+ and DCX+ cells in SGZ. We also tested several depression and anxiety-related behavioral responses whose patter of response observed in KO and OE mice could be related to the differential neurogenetic changes observed.