Dysbindin-1 and schizophrenia: from genetics to neuropathology
J. Clin. Invest. Michael J. Owen, et al. 113:1255 doi:10.1172/JCI21470 [Go to this article.]

Figure 1
Schematic representation of a glutamatergic synapse. Several genes have been implicated in susceptibility to schizophrenia that can potentially impact on glutamate (Glu) synaptic function including dysbindin-1, neuregulin 1 (NRG1), G72, D-amino acid oxidase (DAAO), and regulator of G protein signalling 4 (RGS4). Dysbindin-1 may influence VGlutT-1 expression, synthesis, or degradation and is a component of the postsynaptic density (PSD). NRG1 is present in glutamate synaptic vesicles, regulates expression of N-methyl-D-aspartate receptors (NMDARs), activates ErbB4 receptors, which colocalize with NMDARs, and interacts with the PSD. G72 interacts with DAAO, which oxidizes D-serine, an endogenous modulator of NMDARs. RGS4 is a negative regulator of G protein_coupled receptors, especially the metabotropic glutamate receptor 5 (mGluR5), via its effects on the G protein Gq. Figure modified with permission from The Lancet (7).