Moghaddam Bita, Jackson Mark E
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.
Ann N Y Acad Sci. 2003 Nov;1003:131-7. doi: 10.1196/annals.1300.065.
Several lines of evidence, including recent genetic linkage studies implicating susceptibility genes for schizophrenia, make a strong case that abnormal NMDA receptor-mediated neurotransmission is a major locus for the pathophysiology of schizophrenia. Animal models that are relevant to putative NMDA dysfunction in schizophrenia have excellent face validity for several symptoms of schizophrenia and are important tools for the design of novel pharmacological intervention in schizophrenia. The present chapter includes a brief review of the utility of these models and the search for new medications that have the potential of normalizing glutamate neurotransmission in schizophrenia.
包括近期涉及精神分裂症易感基因的遗传连锁研究在内的多条证据，有力地表明异常的N-甲基-D-天冬氨酸（NMDA）受体介导的神经传递是精神分裂症病理生理学的主要位点。与精神分裂症中假定的NMDA功能障碍相关的动物模型对精神分裂症的几种症状具有出色的表面效度，并且是设计精神分裂症新型药物干预措施的重要工具。本章简要回顾了这些模型的效用以及寻找有可能使精神分裂症中谷氨酸神经传递正常化的新药物。
