The process of adult neurogenesis, ranging from proliferation of neural stem cells to development of their neuronal progeny, is governed by both extrinsic niche signals and intrinsic cellular properties (Ihrie and Alvarez-Buylla, 2011; Ming and Song, 2011). Among extrinsic factors, neurotransmitter γ-aminobutyric acid (GABA) regulates the proliferation of neural progenitors and new neuron development in the adult brain (Ge et al., 2007; Platel et al., 2010). As a classic inhibitory neurotransmitter, GABA hyperpolarizes mature neurons, which maintain low intracellular chloride content ([Cl−]i) through high level expression of a neuronal K+-Cl− co-transporter (KCC2, a Cl− exporter) (Owens and Kriegstein, 2002). In contrast, immature neurons are depolarized by GABA due to their high [Cl−]i as a result of high level expression of a Na+-K+-2Cl− co-transporter (NKCC1, a Cl− importer). Down-regulating NKCC1 or up-regulating KCC2 in immature neurons abolishes GABA-induced depolarization, resulting in defects in dendritic growth and synapse formation during both embryonic and adult neurogenesis (Ge et al., 2007; Platel et al., 2010). Among intrinsic regulators of adult neurogenesis, Disrupted-in-Schizophrenia 1 (DISC1) controls multiple aspects of neuronal development (Ming and Song, 2009).
