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pubmed:abstractText |
Certain cognitive deficits in individuals with schizophrenia have been linked to disturbed gamma-aminobutyric acid (GABA) and glutamate neurotrans-mission in the prefrontal cortex. Thus, it is important to understand how the mechanisms that regulate GABA and glutamate neurotransmission are altered in schizophrenia. For example, group I metabo-tropic glutamate receptors (mGluR1?, mGluR5) modulate both GABA and gluta-mate systems. In addition, regulator of G protein signaling 4 (RGS4) reduces intra-cellular signaling through several different G protein-coupled receptors, including group I mGluRs. Finally, the endocannabinoid system plays an important role in regulating GABA and glutamate neurotrans-mission. The status of endocannabinoid ligands, such as 2-arachidonoylglycerol, can be inferred in part through measures of diacylglycerol lipase and monoglyceride lipase, which synthesize and degrade 2-arachidonoylglycerol, respectively.
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