Role of astrocytes in alterations of glutamatergic neurotransmission in schizophrenia
Abstract The glutamatergic hypothesis of schizophrenia based on the hypofunction of the N-methyl-D-aspartate-type glutamate receptors (NMDA-R) is one of the most widely implicated hypothesis that explains the origin of positive and negative symptoms of illness as well as cognitive deficits. The author considered a neuromorphological aspect of this hypothesis related to the glial astrocytes function. The literature on the astrocyte ability to regulate glutamate neurotransmission is reviewed. Astrocyte abnormalities in schizophrenia include the disturbances of glutamate reuptake, recycling and turnover of endogenous NMDA-R ligands. The results of the experimental and clinical studies that target levels of endogenous NMDA-R ligands, their enzymes and transporters for treatment of schizophrenia symptoms are discussed. Further studies studies are needed to develop this strategy.