Nov 1, 1989

Excitatory amino acid-induced toxicity in chick retina: amino acid release, histology, and effects of chloride channel blockers

Journal of Neurochemistry
G D ZeevalkW J Nicklas

Abstract

Acute excitotoxicity in embryonic chick retina and the ability of Cl- channel blockers to prevent toxicity were evaluated by measurement of endogenous amino acid release and histology. Treatment of retina with kainate, quisqualate, or N-methyl-D-aspartate resulted in a large dose-dependent release of gamma-aminobutyric acid and taurine, moderate release of glutamine and alanine, and no measurable release of glutamate or aspartate. Concentrations inducing maximal gamma-aminobutyric acid release were 50 microM quisquaalate, 100 microM kainate, and 100 microM N-methyl-D-aspartate. Treatment with 1 mM glutamate resulted in significant gamma-aminobutyric acid release, as well as an elevation in medium aspartate levels. Typical excitotoxic retinal lesions were produced by the agonists and, at the lower concentrations tested, revealed a regional sensitivity. There was a positive correlation between the amount of gamma-aminobutyric acid release and the extent of tissue swelling, suggesting that release may be secondary to toxic cellular events. Omission of Cl- completely blocked cytotoxic effects due to kainate or glutamate. Likewise, addition of the Cl-/bicarbonate anion channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonate a...Continue Reading

Mentioned in this Paper

Chloride Ion Level
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Congenital Chloride Diarrhea
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid, Disodium Salt
Salix - substance
Ion Channel
Calcium-Activated Chloride Channels
Retina
Chick Embryo
Drug-Induced Liver Injury

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