Abstract |
Postmortem studies, using various methods and directed at several molecular targets, have provided increasing evidence that glutamatergic neurotransmission is affected in schizophrenia. The bulk of the data are in the hippocampus, wherein there is reduced expression of one or more subunits for all three ionotropic receptors (NMDA, AMPA, and kainate). Presynaptic glutamatergic markers, notably the vesicular glutamate transporter VGLUT1, may also be decreased in schizophrenia, especially in older subjects. CA1 appears less affected than other subfields, and the decrements may be greater in the left than in the right hippocampus. The recently described susceptibility genes for schizophrenia all act upon glutamatergic synaptic transmission, which may, therefore, be part of the core pathophysiology of the disorder.
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Authors | Paul J Harrison, Amanda J Law, Sharon L Eastwood |
Journal | Annals of the New York Academy of Sciences
(Ann N Y Acad Sci)
Vol. 1003
Pg. 94-101
(Nov 2003)
ISSN: 0077-8923 [Print] United States |
PMID | 14684437
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Amino Acid Transport System X-AG
- Glutamates
- Receptors, Glutamate
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Topics |
- Amino Acid Transport System X-AG
(metabolism, physiology)
- Disease Progression
- Functional Laterality
(physiology)
- Glutamates
(physiology)
- Hippocampus
(metabolism)
- Humans
- Receptors, Glutamate
(metabolism, physiology)
- Schizophrenia
(metabolism)
- Synapses
(physiology)
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