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Study of the Mechanism of Release of [ 3 H]GABA from a Teleost Retina In Vitro
Author(s) -
Jaffé E. H.,
Hernández N.,
Holder L. G.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb05377.x
Subject(s) - veratridine , depolarization , nipecotic acid , biophysics , tetrodotoxin , gamma aminobutyric acid , chemistry , potassium , glycine , biochemistry , neurotransmitter , biology , sodium , amino acid , sodium channel , receptor , organic chemistry
γ‐Aminobutyric acid (GABA) is thought to be a neurotransmitter in the vetebrate retina. We studied the voltage and Ca 2+ dependency of the process of release of [ 3 H]GABA from the retina of the teleost Eugenes plumieri , using a microsuperfusion technique. Two depolarizing agents, veratridine and high potassium, produced a concentration‐dependent release of [ 3 H]GABA. The veratridine effect was inhibited in Na + ‐free solution, but was not affected by 1 μ M tetrodotoxin. A substantial inhibition (about 75%) of the veratridine‐and potassium‐stimulated release of [ 3 H] GABA occurred in Ca 2+ ‐free medium. Inhibitors of the Ca 2+ channel, such as Mg 2+ (20 m M ), La 3+ (0.1 m M ), and methoxy‐verapamil (4 μ M ‐0.4 m M ), inhibited the veratridine‐and K + ‐stimulated release. However, Co 2+ and Cd 2+ caused a potentiation and no change of the K + ‐and veratridine‐stimulated release, respectively. This release process is apparently specific, since both depolarizing agents were unable to release [ 3 H]methionine, a nontransmitter amino acid, under the same experimental conditions. Autoradio‐graphic studies with [ 3 H]GABA, using the same incubation conditions as for the release experiments, showed a high density of silver grains over the horizontal cells with almost no accumulation by amacrine cells and Muller cells. β‐Alanine and nipecotic acid were used as two relative specific inhibitors of the glial and neuronal GABA uptake mechanisms, respectively. Only a small heteroexchange with [ 3 H]GABA was found with β‐alanine, and no inhibition of the subsequent veratridine‐stimulated release. On the other hand, nipecotic acid produced a strong heteroexchange with [ 3 H]GABA and lacked the capacity to induce the veratridine‐stimulated release of [ 3 H]GABA. These results suggest a voltage‐and Ca 2+ ‐dependent neuronal release of [ 3 H]GABA from retina.