Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.

Excitotoxicity has been implicated in the retinal neuronal loss in several ocular pathologies including glaucoma. Dysfunction of Excitatory Amino Acid Transporters is often a key component of the cascade leading to excitotoxic cell death. In the retina, glutamate transport is mainly operated by the...

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Autores principales:	Rossella Russo, Federica Cavaliere, Giuseppe Pasquale Varano, Marco Milanese, Annagrazia Adornetto, Carlo Nucci, Giambattista Bonanno, Luigi Antonio Morrone, Maria Tiziana Corasaniti, Giacinto Bagetta
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b4628a424d2a44208b0690cceba3ce28
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spelling	oai:doaj.org-article:b4628a424d2a44208b0690cceba3ce282021-11-18T09:01:03ZImpairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.1932-620310.1371/journal.pone.0069250https://doaj.org/article/b4628a424d2a44208b0690cceba3ce282013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23936321/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Excitotoxicity has been implicated in the retinal neuronal loss in several ocular pathologies including glaucoma. Dysfunction of Excitatory Amino Acid Transporters is often a key component of the cascade leading to excitotoxic cell death. In the retina, glutamate transport is mainly operated by the glial glutamate transporter GLAST and the neuronal transporter GLT-1. In this study we evaluated the expression of GLAST and GLT-1 in a rat model of acute glaucoma based on the transient increase of intraocular pressure (IOP) and characterized by high glutamate levels during the reperfusion that follows the ischemic event associated with raised IOP. No changes were reported in GLAST expression while, at neuronal level, a reduction of glutamate uptake and of transporter reversal-mediated glutamate release was observed in isolated retinal synaptosomes. This was accompanied by modulation of GLT-1 expression leading to the reduction of the canonical 65 kDa form and upregulation of a GLT-1-related 38 kDa protein. These results support a role for neuronal transporters in glutamate accumulation observed in the retina following an ischemic event and suggest the presence of a GLT-1 neuronal new alternative splice variant, induced in response to the detrimental stimulus.Rossella RussoFederica CavaliereGiuseppe Pasquale VaranoMarco MilaneseAnnagrazia AdornettoCarlo NucciGiambattista BonannoLuigi Antonio MorroneMaria Tiziana CorasanitiGiacinto BagettaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e69250 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rossella Russo Federica Cavaliere Giuseppe Pasquale Varano Marco Milanese Annagrazia Adornetto Carlo Nucci Giambattista Bonanno Luigi Antonio Morrone Maria Tiziana Corasaniti Giacinto Bagetta Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
description	Excitotoxicity has been implicated in the retinal neuronal loss in several ocular pathologies including glaucoma. Dysfunction of Excitatory Amino Acid Transporters is often a key component of the cascade leading to excitotoxic cell death. In the retina, glutamate transport is mainly operated by the glial glutamate transporter GLAST and the neuronal transporter GLT-1. In this study we evaluated the expression of GLAST and GLT-1 in a rat model of acute glaucoma based on the transient increase of intraocular pressure (IOP) and characterized by high glutamate levels during the reperfusion that follows the ischemic event associated with raised IOP. No changes were reported in GLAST expression while, at neuronal level, a reduction of glutamate uptake and of transporter reversal-mediated glutamate release was observed in isolated retinal synaptosomes. This was accompanied by modulation of GLT-1 expression leading to the reduction of the canonical 65 kDa form and upregulation of a GLT-1-related 38 kDa protein. These results support a role for neuronal transporters in glutamate accumulation observed in the retina following an ischemic event and suggest the presence of a GLT-1 neuronal new alternative splice variant, induced in response to the detrimental stimulus.
format	article
author	Rossella Russo Federica Cavaliere Giuseppe Pasquale Varano Marco Milanese Annagrazia Adornetto Carlo Nucci Giambattista Bonanno Luigi Antonio Morrone Maria Tiziana Corasaniti Giacinto Bagetta
author_facet	Rossella Russo Federica Cavaliere Giuseppe Pasquale Varano Marco Milanese Annagrazia Adornetto Carlo Nucci Giambattista Bonanno Luigi Antonio Morrone Maria Tiziana Corasaniti Giacinto Bagetta
author_sort	Rossella Russo
title	Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
title_short	Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
title_full	Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
title_fullStr	Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
title_full_unstemmed	Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.
title_sort	impairment of neuronal glutamate uptake and modulation of the glutamate transporter glt-1 induced by retinal ischemia.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/b4628a424d2a44208b0690cceba3ce28
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Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia.

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