期刊
YEAR IN NEUROLOGY AND PSYCHIATRY
卷 1338, 期 -, 页码 38-57出版社
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12547
关键词
brain tissue; EAAT; glutamate receptors; glutamatergic neurons; schizophrenia
资金
- NIMH NIH HHS [P50 MH103204, MH 16804, MH 071533, T32 MH016804, R21 MH066231, R01 MH071533, MH 103204] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH103204, R01MH071533, R21MH066231, T32MH016804] Funding Source: NIH RePORTER
A number of studies have indicated that antagonists of the N-methyl-d-aspartate subtypes of glutamate receptors can cause schizophrenia-like symptoms in healthy individuals and exacerbate symptoms in individuals with schizophrenia. These findings have led to the glutamate hypothesis of schizophrenia. Here we review the evidence for this hypothesis in postmortem studies of brain tissue from individuals affected by schizophrenia, summarizing studies of glutamate neuron morphology, of expression of glutamate receptors and transporters, and of the synthesizing and metabolizing enzymes for glutamate and its co-agonists. We found consistent evidence of morphological alterations of dendrites of glutamatergic neurons in the cerebral cortex of subjects with schizophrenia and of reduced levels of the axon bouton marker synaptophysin. There were no consistent alterations of mRNA expression of glutamate receptors, although there has been limited study of the corresponding proteins. Studies of the glutamate metabolic pathway have been limited, although there is some evidence that excitatory amino acid transporter-2, glutamine synthetase, and glutaminase have altered expression in schizophrenia. Future studies would benefit from additional direct examination of glutamatergic proteins. Further advances, such as selective testing of synaptic microdomains, cortical layers, and neuronal subtypes, may also be required to elucidate the nature of glutamate signaling impairments in schizophrenia.
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