May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Retinal Excitatory Amino Acid Transporters Are Continually Expressed Following Acute Ischaemia
Author Affiliations & Notes
  • N.L. Barnett
    Vision Touch & Hearing Research Centre, The University of Queensland, Brisbane, Australia
  • S.D. Grozdanic
    Dept of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA, United States
  • R.A. Allbaugh
    Dept of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA, United States
  • Footnotes
    Commercial Relationships  N.L. Barnett, None; S.D. Grozdanic, None; R.A. Allbaugh, None.
  • Footnotes
    Support  NHMRC (Australia), The Glaucoma Foundation, NY.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2936. doi:https://doi.org/
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      N.L. Barnett, S.D. Grozdanic, R.A. Allbaugh; Retinal Excitatory Amino Acid Transporters Are Continually Expressed Following Acute Ischaemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2936. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

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.

Keywords: ischemia • excitatory neurotransmitters • retina: neurochemistry 
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