of neuronal development driven by prolonged GABA-mediated depolarization. Multiple neurotransmitters, including GABA, have been shown to activate the AKT pathway through Ca2+ signaling (Yano et al., 1998). Using a series of genetic, pharmacological and immunohistological approaches, we provided evidence supporting the model that AKT serves as a point of convergence and DISC1 gates depolarizing GABA-induced AKT/mTOR signaling to regulate dendritic growth of newborn neurons in a context-dependent fashion (Figures 5E to 5F). Given DISC1 interacts with many partners, it is possible that DISC1 also gates other signaling pathways in regulating different aspects of neuronal development and function.
