期刊
CURRENT PHARMACEUTICAL DESIGN
卷 18, 期 12, 页码 1593-1604出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161212799958576
关键词
NMDA; DISC1; phencyclidine; antipsychotic drugs; metabotropic glutamate receptors
资金
- NIMH NIH HHS [R37 MH048404] Funding Source: Medline
- NINDS NIH HHS [F33 NS010855] Funding Source: Medline
Dysregulation of glutamate neurotransmission has been implicated in schizophrenia primarily because antagonists of the n-methyl-d-aspartate (NMDA) subtype of glutamate receptors exacerbate preexisting symptoms of schizophrenia in patients and produce behavioral disruptions that resemble some symptoms of schizophrenia in healthy individuals. Given this, NMDA receptor antagonists have been used extensively to model aspects of the disease in laboratory animals and have provided a useful preclinical tool for testing novel treatment strategies. More recent genetic and postmortem findings have implicated proteins other than the NMDA receptor in the pathophysiology of schizophrenia which play a role in regulation of the glutamate synapse. Animal models developed based on these findings have the potential of increasing our mechanistic understanding of the disease. Here we review some of the pertinent literature related to pharmacological and genetic animal models of glutamate dysfunction in schizophrenia.
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