The glutamate synapse in neuropsychiatric disorders: Focus on schizophrenia and Alzheimer's disease

N. B. Farber, J. W. Newcomer, J. W. Olney

Research output: Contribution to journalReview article

133 Scopus citations

Abstract

Here we have described a novel excitotoxic process in which hypofunctional NMDA receptors cease driving GABAergic neurons which cease inhibiting excitatory transmitters in the brain. These disinhibited excitatory transmitters then act in concert to slowly hyperstimulate neurons in corticolimbic brain regions. We have discussed how such an abnormality could exist in the brains of individuals with schizophrenia or AD and could account for the clinical stigmata of the two disorders. In addition, we have highlighted how other disorder-specific factors would account for the differences in the clinical presentation of AD and schizophrenia. In an animal model, pharmacological methods have been developed for preventing the overstimulation of these vulnerable corticolimbic pyramidal neurons and at least some of these methods may be applicable for treating AD and schizophrenia.

Original languageEnglish
Pages (from-to)421-437
Number of pages17
JournalProgress in Brain Research
Volume116
StatePublished - Jan 1 1998

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