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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Language: | English |
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Wiley
2013-01-01
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Series: | Scientifica |
Online Access: | http://dx.doi.org/10.1155/2013/528940 |
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author | Makoto Ishikawa |
author_facet | Makoto Ishikawa |
author_sort | Makoto Ishikawa |
collection | DOAJ |
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 | Article |
id | doaj-art-4404d8f1578c43288a4c8a5723a2b2a1 |
institution | Kabale University |
issn | 2090-908X |
language | English |
publishDate | 2013-01-01 |
publisher | Wiley |
record_format | Article |
series | Scientifica |
spelling | doaj-art-4404d8f1578c43288a4c8a5723a2b2a12025-02-03T01:06:52ZengWileyScientifica2090-908X2013-01-01201310.1155/2013/528940528940Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal DiseasesMakoto Ishikawa0Department of Ophthalmology, Akita Graduate University Faculty of Medicine, 1-1-1 Hondo, Akita 010-8543, JapanIn 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.http://dx.doi.org/10.1155/2013/528940 |
spellingShingle | Makoto Ishikawa Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases Scientifica |
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 |
url | http://dx.doi.org/10.1155/2013/528940 |
work_keys_str_mv | AT makotoishikawa abnormalitiesinglutamatemetabolismandexcitotoxicityintheretinaldiseases |