If the entire retina of an experimental animal is subjected to ischemia for a certain period of time and is then reperfused, subsequent cell death occurs particularly in the inner part of the retina, manifesting in a delayed fashion (Fig. 1). This delayed neuronal death due to retinal ischemia is now believed to reflect impaired cellular ion homeostasis especially concerning Ca2+.
KeywordsNitric Oxide NMDA Receptor Amacrine Cell Ganglion Cell Layer Outer Nuclear Layer
Unable to display preview. Download preview PDF.
- Hedges TR (1962) Ophthalmoscopic findings in internal cartotid occlusion. Bull Johns Hopkins Hosp 3:89–97Google Scholar
- Kashii S (1995) The role of nitric oxide in the ischemic retina. J Jpn Ophthalmol Soc 99:1361–1376Google Scholar
- Kearns TP, Hollenhorst RW (1963) Venous-stasis retinopathy of occlusive disease of the carotid artery. Mayo Clin Proc 38:304–312Google Scholar
- Louzada JP, Dias JJ, Santos WF, Lachat JJ, Bradford HF, Coutinho NJ (1992) Glutamate release in experimental ischemia of the retina: an approach using microdialysis. J Neu-rochem 59:358–363Google Scholar
- Miller NR (1991) Walsh and Hoyt’s clinical neuro-ophthalmology (4th ed). Williams & Wilkins, Baltimore, pp 2336–2344Google Scholar
- Schwarcz R, Coyle JT (1977) Kainic acid: neurotoxic efects after intraocular injection. Invest Ophthalmol 16:141–148Google Scholar
- Uchiyama TY, Araki H, Tae T, Otomo S (1994) Changes in the extracellular concentrations of amino acids in the rat striatum during transient focal cerebral ischemia. J Neu-rochem 62:1074–1078Google Scholar