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Evidence for the Action of Endogenous Adenosine in the Rabbit Retina: Modulation of the Light‐Evoked Release of Acetylcholine
Author(s) -
Blazynski Christine,
Woods Cynthia,
Mathews Gregory C.
Publication year - 1992
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.1471-4159.1992.tb09783.x
Subject(s) - adenosine , adenosine deaminase , acetylcholine , purinergic signalling , adenosine a1 receptor , retina , adenosine receptor , nucleoside , endocrinology , agonist , medicine , cholinergic , chemistry , biology , adenosine a3 receptor , pharmacology , biochemistry , receptor , neuroscience
Much evidence has accumulated supporting the hypothesis that the purine nucleoside adenosine may indeed function as a neuromodulator in the mammalian retina, but to date no reports have directly illustrated a physiological role for this nucleoside. In other regions of the CNS, adenosine agonists decrease transmitter release, whereas antagonists increase release. A similar role for adenosine in the retina is now apparent. The cholinergic amacrine cells of the rabbit retina were labeled with [ 3 H]choline, and the effects of enzymatic adenosine degradation or adenosine antagonists on the light‐evoked efflux of acetylcholine were evaluated. When endogenous adenosine was degraded by addition of adenosine deaminase, the light‐evoked release of radioactivity derived from [ 3 H]choline was significantly increased compared with control values. A similar response was observed when rabbit eyecups were superfused with a selective adenosine A 1 receptor antagonist. The effect elicited by adenosine deaminase could be almost completely reversed by addition of cyclo‐pentyladenosine, a highly selective A 1 receptor agonist. These effects were observed in either the presence or the absence of picrotoxin. The results demonstrate a modulation of retinal physiology by adenosine.