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N-甲基-D-天冬氨酸受体与精神分裂症

NMDA receptors and schizophrenia.

作者信息

Kristiansen Lars V, Huerta Ibone, Beneyto Monica, Meador-Woodruff James H

机构信息

University of Alabama at Birmingham, Department of Psychiatry and Behavioral Neurobiology, SC560, 1530 3rd Avenue South, Birmingham, AL 35294-0017, USA.

出版信息

Curr Opin Pharmacol. 2007 Feb;7(1):48-55. doi: 10.1016/j.coph.2006.08.013. Epub 2006 Nov 9.

DOI:10.1016/j.coph.2006.08.013
PMID:17097347
Abstract

The pathophysiology of schizophrenia is poorly understood but is likely to involve alterations in excitatory glutamatergic signaling molecules in several areas of the brain. Clinical and experimental evidence has shown that expression of the N-methyl-D-aspartate (NMDA) receptor and intracellular NMDA receptor-interacting proteins of the glutaminergic synapse appear to be dysregulated in schizophrenia. It has been suggested that schizophrenia involves molecular changes in the glutamatergic pathways that mediate excitatory communication between multiple brain regions. Recent data also implicate abnormalities in cellular functions such as receptor trafficking and synaptic targeting.

摘要

精神分裂症的病理生理学仍未被充分理解,但可能涉及大脑多个区域兴奋性谷氨酸能信号分子的改变。临床和实验证据表明,精神分裂症患者中,谷氨酸能突触的N-甲基-D-天冬氨酸(NMDA)受体及细胞内与NMDA受体相互作用的蛋白质的表达似乎失调。有人提出,精神分裂症涉及谷氨酸能通路中的分子变化,这些通路介导多个脑区之间的兴奋性通讯。最近的数据还表明细胞功能存在异常,如受体运输和突触靶向。

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