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Phenomenology, aetiology and treatment of schizophrenia.

Daniel C Javitt

Novartis Foundation symposium 2008 DOI: 10.1002/9780470751251.ch2 (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Philosophy of mind
Key findings Glutamatergic models of schizophrenia, based on NMDA receptor blockade by PCP and ketamine, account for features poorly explained by dopaminergic dysfunction alone and may lead to new treatments.

Abstract

Schizophrenia is a serious mental disorder that affects up to 1% of the population worldwide. Traditional models of schizophrenia have emphasized dopaminergic dysfunction. Over the last 15 years, however, glutamatergic models have become increasingly mainstream, and account for features of the disorder that are poorly explained by dopaminergic dysfunction alone. Glutamatergic models, such as the PCP/NMDA model, are based upon the observation that the psychotomimetic agents phencyclidine (PCP) and ketamine induce psychotic symptoms and neurocognitive disturbances similar to those of schizophrenia by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors. Because NMDA receptors are located throughout the brain, information-processing deficits are observed not only in higher cortical regions, but also in sensory cortices and subcortical systems. Further, NMDA receptors are located on brain circuits that regulate dopamine release, suggesting that dopaminergic deficits in schizophrenia may also be secondary to underlying glutamatergic dysfunction. Agents that stimulate glutamatergic neurotransmission, including glycine-site agonists and glycine transport inhibitors, have shown encouraging results in preclinical studies and are currently undergoing clinical development. Overall, these findings suggest that glutamatergic theories may lead to new conceptualizations and treatment approaches that would not be possible based upon dopaminergic models alone.

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