Glutamatergic Animal Models of Schizophrenia

Authors

  • BITA MOGHADDAM,

    Corresponding author
    1. Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA
      Address for correspondence: Bita Moghaddam, Department of Neuroscience, University of Pittsburgh, 446 Crawford Hall, Pittsburgh, PA 15260. Voice: 412-624-2653; fax: 412-624-9198. bita@pitt.edu
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  • MARK E. JACKSON

    1. Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA
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Address for correspondence: Bita Moghaddam, Department of Neuroscience, University of Pittsburgh, 446 Crawford Hall, Pittsburgh, PA 15260. Voice: 412-624-2653; fax: 412-624-9198. bita@pitt.edu

Abstract

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.

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