The past decade has been characterized by a significant change in the approach of psychologists and neuroscientists to the study of psychopathology (Cicchetti, 1993; Cicchetti & Cannon, 1999) and how we conceptualize the etiology of mental illness during childhood, adolescence, and adulthood (Benes, 1995). Among these disorders, schizophrenia and, more recently, bipolar disorder have received the most attention with recent postmortem studies having provided compelling evidence for a defect of GABAergic neurotransmission playing a role in its pathophysiology (for a review, see Benes & Berretta, 2001). For example, findings of a decreased density of interneurons (Benes, McSparren, Bird, SanGiovanni, & Vincent, 1991; Benes, Kwok, Vincent, & Todtenkopf, 1998), reduced GABA uptake (Simpson et al., 1989; Reynolds, Czudek, & Andrews, 1990), increased GABA receptor binding activity (Benes, Khan, Vincent, & Wickramasinghe, 1996; Benes, Vincent, Alsterberg, Bird, & SanGiovanni, 1992), decreased GABA terminals (Benes, Todtenkopf, Logiotatos, & Williams, 2000), and reduced expression of mRNA for GAD65 and GAD67 (Akbarian et al., 1995; Guidotti et al., 2000; Heckers et al., 2001; Volk, Austin, Pierri, Sampson, & Lewis, 2000) reported to date are consistent with the idea that there may be a decrease of GABAergic cells and/or activity in these disorders. Since the mechanism of action of antipsychotic medication involves blockade of both dopamine and serotonin receptors (Meltzer, 1994), a key question is how GABA cells interact with these monoaminergic systems in corticolimbic regions of schizophrenic brain.