Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autor principal: Ishikawa, Makoto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
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
_version_ 1782296964156620800
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