Glutamatergic Animal Models of Schizophrenia

Bita Moghaddam, Mark E. Jackson

Research output: Contribution to journalArticlepeer-review

125 Scopus citations


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 languageEnglish (US)
Pages (from-to)131-137
Number of pages7
JournalAnnals of the New York Academy of Sciences
StatePublished - Nov 2003
Externally publishedYes


  • 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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