Glutamatergic Animal Models of Schizophrenia

Bita Moghaddam; Mark E. Jackson

doi:10.1196/annals.1300.065

Glutamatergic Animal Models of Schizophrenia

Bita Moghaddam, Mark E. Jackson

Research output: Contribution to journal › Article › peer-review

126 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	131-137
Number of pages	7
Journal	Annals of the New York Academy of Sciences
Volume	1003
DOIs	https://doi.org/10.1196/annals.1300.065
State	Published - Nov 2003
Externally published	Yes

Keywords

Cognitions
Dopamine
NMDA receptors
Prefrontal cortex
Schizophrenia

ASJC Scopus subject areas

General Neuroscience
General Biochemistry, Genetics and Molecular Biology
History and Philosophy of Science

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10.1196/annals.1300.065

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AB - 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.

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Glutamatergic Animal Models of Schizophrenia

Abstract

Keywords

ASJC Scopus subject areas

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