BACLOFEN ENHANCEMENT OF ACETYLCHOLINE-RELEASE FROM AMACRINE CELLS IN THE RABBIT RETINA BY REDUCTION OF GLYCINERGIC INHIBITION

1. The mechanism by which the GABA(B)-receptor agonist, baclofen, enha nces the light-evoked release of [H-3]acetylcholine (ACh) from choline rgic amacrine cells was studied using an eye-cup preparation in anaest hetized rabbits and isolated retinas. 2. When applied locally to the r abbit retina, baclofen increased the release of ACh evoked by a flicke ring light (3 Hz) by over 40 %. 3. In isolated retinas, baclofen strik ingly inhibited the K+-evoked release of glycine but had no effect on GABA release. 4. In the rabbit eye cup, strychnine enhanced the light- evoked release of ACh to a similar degree to that produced by baclofen . The effects of baclofen and strychnine on the light-evoked release o f ACh mere not additive. In contrast, bicuculline did not affect the e nhancing action of baclofen on the light-evoked release of ACh. 5. In order to see whether the glycinergic amacrine cells might be stimulate d by ACh, isolated rat and rabbit retinas were exposed to muscarine. T his cholinergic agonist potentiated the K+-evoked release of glycine b y 54 %. 6. We suggest that baclofen enhances the light-evoked release of ACh from amacrine cells by inhibiting glycine release from glyciner gic amacrine cells which are stimulated by ACh and form an inhibitory feedback loop to the cholinergic neurones.