Retinal excitatory amino acid transporters are continually expressed following acute ischaemia

NL Barnett, SD Grozdanic, RA Allbaugh

Research output: Contribution to journalMeeting AbstractResearchpeer-review

Abstract

Purpose: To assess the long term expression of excitatory amino acid transporters (EAATs) following an acute ischaemic insult to the retina. In the retina, EAATs maintain the extracellular concentration of glutamate below excitotoxic levels. However, following an ischaemic insult, glutamate concentrations rise and contribute to excitotoxic neurodegeneration. Here we studied the expression of the retinal EAATs i.e. GLAST, Glt-1, EAAC1 and EAAT5 for 60 days after an acute ischaemic insult. Methods: Adult Brown Norway rats were anesthetised with 2.5% halothane, 30% nitrous oxide and 70% oxygen. After topical instillation of 0.5% propracaine hydrochloride, the anterior chamber was cannulated with a 25-gauge needle connected to a reservoir containing 0.9% NaCl. The intraocular pressure in experimental eyes was controlled by the height of the reservoir to maintain a pressure of 110 mmHg to induce acute ischaemia for 60 minutes. After this period, the needle was removed to allow reperfusion for 10, 25, 35, 45 or 60 days. Results: Intense immunoreactivity for GLAST (Müller cells), Glt-1 (cone photoreceptor and bipolar cells) and EAAT5 (rod photoreceptor and bipolar cells) was observed at all time points after the insult, despite severe retinal degeneration. EAAC1 immunoreactive amacrine and ganglion cells declined in number but not intensity over time, reflecting the loss of these cells following ischaemia. Conclusions: These data suggest that ischaemic retinal degeneration is not due to suppressed excitatory amino acid transporter expression.
Original languageEnglish
Article number2936
Pages (from-to)U81
JournalInvestigative Ophthalmology
Volume44
Issue number13
Publication statusPublished - May 2003
Externally publishedYes
EventAnnual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology - FT LAUDERDALE
Duration: 4 May 2003 → …

Cite this

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title = "Retinal excitatory amino acid transporters are continually expressed following acute ischaemia",
abstract = "Purpose: To assess the long term expression of excitatory amino acid transporters (EAATs) following an acute ischaemic insult to the retina. In the retina, EAATs maintain the extracellular concentration of glutamate below excitotoxic levels. However, following an ischaemic insult, glutamate concentrations rise and contribute to excitotoxic neurodegeneration. Here we studied the expression of the retinal EAATs i.e. GLAST, Glt-1, EAAC1 and EAAT5 for 60 days after an acute ischaemic insult. Methods: Adult Brown Norway rats were anesthetised with 2.5{\%} halothane, 30{\%} nitrous oxide and 70{\%} oxygen. After topical instillation of 0.5{\%} propracaine hydrochloride, the anterior chamber was cannulated with a 25-gauge needle connected to a reservoir containing 0.9{\%} NaCl. The intraocular pressure in experimental eyes was controlled by the height of the reservoir to maintain a pressure of 110 mmHg to induce acute ischaemia for 60 minutes. After this period, the needle was removed to allow reperfusion for 10, 25, 35, 45 or 60 days. Results: Intense immunoreactivity for GLAST (M{\"u}ller cells), Glt-1 (cone photoreceptor and bipolar cells) and EAAT5 (rod photoreceptor and bipolar cells) was observed at all time points after the insult, despite severe retinal degeneration. EAAC1 immunoreactive amacrine and ganglion cells declined in number but not intensity over time, reflecting the loss of these cells following ischaemia. Conclusions: These data suggest that ischaemic retinal degeneration is not due to suppressed excitatory amino acid transporter expression.",
author = "NL Barnett and SD Grozdanic and RA Allbaugh",
year = "2003",
month = "5",
language = "English",
volume = "44",
pages = "U81",
journal = "Investigative Ophthalmology",
issn = "0146-0404",
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}

Retinal excitatory amino acid transporters are continually expressed following acute ischaemia. / Barnett, NL; Grozdanic, SD; Allbaugh, RA.

In: Investigative Ophthalmology, Vol. 44, No. 13, 2936, 05.2003, p. U81.

Research output: Contribution to journalMeeting AbstractResearchpeer-review

TY - JOUR

T1 - Retinal excitatory amino acid transporters are continually expressed following acute ischaemia

AU - Barnett, NL

AU - Grozdanic, SD

AU - Allbaugh, RA

PY - 2003/5

Y1 - 2003/5

N2 - Purpose: To assess the long term expression of excitatory amino acid transporters (EAATs) following an acute ischaemic insult to the retina. In the retina, EAATs maintain the extracellular concentration of glutamate below excitotoxic levels. However, following an ischaemic insult, glutamate concentrations rise and contribute to excitotoxic neurodegeneration. Here we studied the expression of the retinal EAATs i.e. GLAST, Glt-1, EAAC1 and EAAT5 for 60 days after an acute ischaemic insult. Methods: Adult Brown Norway rats were anesthetised with 2.5% halothane, 30% nitrous oxide and 70% oxygen. After topical instillation of 0.5% propracaine hydrochloride, the anterior chamber was cannulated with a 25-gauge needle connected to a reservoir containing 0.9% NaCl. The intraocular pressure in experimental eyes was controlled by the height of the reservoir to maintain a pressure of 110 mmHg to induce acute ischaemia for 60 minutes. After this period, the needle was removed to allow reperfusion for 10, 25, 35, 45 or 60 days. Results: Intense immunoreactivity for GLAST (Müller cells), Glt-1 (cone photoreceptor and bipolar cells) and EAAT5 (rod photoreceptor and bipolar cells) was observed at all time points after the insult, despite severe retinal degeneration. EAAC1 immunoreactive amacrine and ganglion cells declined in number but not intensity over time, reflecting the loss of these cells following ischaemia. Conclusions: These data suggest that ischaemic retinal degeneration is not due to suppressed excitatory amino acid transporter expression.

AB - Purpose: To assess the long term expression of excitatory amino acid transporters (EAATs) following an acute ischaemic insult to the retina. In the retina, EAATs maintain the extracellular concentration of glutamate below excitotoxic levels. However, following an ischaemic insult, glutamate concentrations rise and contribute to excitotoxic neurodegeneration. Here we studied the expression of the retinal EAATs i.e. GLAST, Glt-1, EAAC1 and EAAT5 for 60 days after an acute ischaemic insult. Methods: Adult Brown Norway rats were anesthetised with 2.5% halothane, 30% nitrous oxide and 70% oxygen. After topical instillation of 0.5% propracaine hydrochloride, the anterior chamber was cannulated with a 25-gauge needle connected to a reservoir containing 0.9% NaCl. The intraocular pressure in experimental eyes was controlled by the height of the reservoir to maintain a pressure of 110 mmHg to induce acute ischaemia for 60 minutes. After this period, the needle was removed to allow reperfusion for 10, 25, 35, 45 or 60 days. Results: Intense immunoreactivity for GLAST (Müller cells), Glt-1 (cone photoreceptor and bipolar cells) and EAAT5 (rod photoreceptor and bipolar cells) was observed at all time points after the insult, despite severe retinal degeneration. EAAC1 immunoreactive amacrine and ganglion cells declined in number but not intensity over time, reflecting the loss of these cells following ischaemia. Conclusions: These data suggest that ischaemic retinal degeneration is not due to suppressed excitatory amino acid transporter expression.

M3 - Meeting Abstract

VL - 44

SP - U81

JO - Investigative Ophthalmology

JF - Investigative Ophthalmology

SN - 0146-0404

IS - 13

M1 - 2936

ER -