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 | |
| State | Published - Nov 2003 |
| Externally published | Yes |
Keywords
- Cognitions
- Dopamine
- NMDA receptors
- Prefrontal cortex
- Schizophrenia
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science