Kolomeets N S
Mental Health Research Center, Russian Academy of Medical Sciences, Moscow.
Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(1):110-117. doi: 10.17116/jnevro201511511110-117.
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.
基于N-甲基-D-天冬氨酸型谷氨酸受体（NMDA-R）功能减退的精神分裂症谷氨酸能假说，是解释该疾病阳性和阴性症状以及认知缺陷起源的最广泛涉及的假说之一。作者考虑了这一假说与神经胶质星形胶质细胞功能相关的神经形态学方面。本文综述了关于星形胶质细胞调节谷氨酸神经传递能力的文献。精神分裂症中的星形胶质细胞异常包括谷氨酸再摄取、内源性NMDA-R配体的循环利用和周转障碍。讨论了针对内源性NMDA-R配体、其酶和转运体水平来治疗精神分裂症症状的实验和临床研究结果。需要进一步研究来发展这一策略。
