Overwhelming genetic evidence now demonstrates that SZ is a complex genetic disorder (Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014) reflecting cumulative risk from more than 100 rare and common variants. Although the genetic and symptomatic heterogeneity of SZ implicates a wide variety of neurotransmitter, neuroimmune, neuroanatomical, and neurodevelopmental processes (reviewed xx), the precise cell type(s) responsible for the cell autonomous defects underlying the earliest disease processes remain unresolved. Historically, the effectiveness of D2-receptor antagonists as anti-psychotics shaped much of the thinking surrounding the neurobiological mechanisms of SZ (Delay et al., 1952; Carlsson et al., 1957); while successful in some cases at alleviating the positive and, to a lesser extent (Kirkpatrick et al., 2001), negative symptoms of SZ, these drugs produce a plethora of side effects which lead to high rates of discontinuation (Lieberman et al., 2005). Glutamatergic signaling via n-methyl-D-aspartate receptor (NMDA-R) has also been repeatedly linked to disordered cognition and sensory processing (for review see Kantrowitz and Javitt, 2012); NMDA-R antagonists, such as phencyclidine and ketamine, mimic some cognitive and behavioral symptoms of SZ (Kehrer et al.,
