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Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases
In the physiological condition, glutamate acts as an excitatory neurotransmitter in the retina. However, excessive glutamate can be toxic to retinal neurons by overstimulation of the glutamate receptors. Glutamate excess is primarily attributed to perturbation in the homeostasis of the glutamate met...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2013
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872404/ https://www.ncbi.nlm.nih.gov/pubmed/24386591 http://dx.doi.org/10.1155/2013/528940 |
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author | Ishikawa, Makoto |
author_facet | Ishikawa, Makoto |
author_sort | Ishikawa, Makoto |
collection | PubMed |
description | In the physiological condition, glutamate acts as an excitatory neurotransmitter in the retina. However, excessive glutamate can be toxic to retinal neurons by overstimulation of the glutamate receptors. Glutamate excess is primarily attributed to perturbation in the homeostasis of the glutamate metabolism. Major pathway of glutamate metabolism consists of glutamate uptake by glutamate transporters followed by enzymatic conversion of glutamate to nontoxic glutamine by glutamine synthetase. Glutamate metabolism requires energy supply, and the energy loss inhibits the functions of both glutamate transporters and glutamine synthetase. In this review, we describe the present knowledge concerning the retinal glutamate metabolism under the physiological and pathological conditions. |
format | Online Article Text |
id | pubmed-3872404 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-38724042014-01-02 Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases Ishikawa, Makoto Scientifica (Cairo) Review Article In the physiological condition, glutamate acts as an excitatory neurotransmitter in the retina. However, excessive glutamate can be toxic to retinal neurons by overstimulation of the glutamate receptors. Glutamate excess is primarily attributed to perturbation in the homeostasis of the glutamate metabolism. Major pathway of glutamate metabolism consists of glutamate uptake by glutamate transporters followed by enzymatic conversion of glutamate to nontoxic glutamine by glutamine synthetase. Glutamate metabolism requires energy supply, and the energy loss inhibits the functions of both glutamate transporters and glutamine synthetase. In this review, we describe the present knowledge concerning the retinal glutamate metabolism under the physiological and pathological conditions. Hindawi Publishing Corporation 2013 2013-12-09 /pmc/articles/PMC3872404/ /pubmed/24386591 http://dx.doi.org/10.1155/2013/528940 Text en Copyright © 2013 Makoto Ishikawa. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Ishikawa, Makoto Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title | Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title_full | Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title_fullStr | Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title_full_unstemmed | Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title_short | Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases |
title_sort | abnormalities in glutamate metabolism and excitotoxicity in the retinal diseases |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872404/ https://www.ncbi.nlm.nih.gov/pubmed/24386591 http://dx.doi.org/10.1155/2013/528940 |
work_keys_str_mv | AT ishikawamakoto abnormalitiesinglutamatemetabolismandexcitotoxicityintheretinaldiseases |