Aberrant neuronal development is believed to contribute to the pathogenesis of mental disorders such as schizophrenia and autism (Geschwind and Levitt, 2007; Lewis and Levitt, 2002; Weinberger, 1987). GABA signaling and DISC1 have both been implicated in schizophrenia and other major mental disorders (Balu and Coyle, 2011). There is strong evidence implicating deficits of GABA signaling in the pathophysiology of schizophrenia (Hyde et al., 2011; Lewis et al., 2005; Perry et al., 1979). Several GABAAR subunits and GAD67 have been linked to increased risk for schizophrenia and related disorders in genetic association studies and many of them exhibit abnormal expression in postmortem patient tissues (Charych et al., 2009; Straub et al., 2007). DISC1 was initially identified at the break-point of a balanced chromosomal translocation (1;11)(q42; q14) that co-segregates with schizophrenia and other major mental illness in a large Scottish family (Millar et al., 2000). Further genetic association studies support an expanded role of DISC1 in influencing risks for schizophrenia, bipolar disorders, major depression, and autism (Chubb et al., 2008). To understand how DISC1 dysfunction contributes to a broad spectrum of
