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., 2008). Another possibility is that the loss of NMDA receptors on GABAergic interneurons leads to hyper-activation of cortical forebrain neurons (Olney et al., 1999), thus leading to an overall excitation/inhibition imbalance (Homayoun and Moghaddam, 2007). Since glutamatergic signaling on GABAergic interneurons has an important regulatory function on the activity of dopaminergic neurons, it seems reasonable that genetic variants impacting any (or all) of these cell types could lead to convergent elements of symptomology across genetically heterogeneous patients.
