Pharmacological identification of retinal cells releasing taurine by light stimulation.

The effect of drugs blocking synaptic activity at different retinal levels was examined in this study, in an attempt to identify the origin of the light-stimulated release of 3H-taurine from the chick retina. It was determined by autoradiography that the chick retina accumulates taurine in photoreceptors, in cells from the inner nuclear layer, and in processes of the inner plexiform layer. All these are possible sites for the release of taurine upon illumination. To discriminate among these possibilities, the effects of aspartate, tetrodotoxin, strychnine, picrotoxin, chlorpromazine, tubocurarine, atropine, glutamate diethyl esther, alpha-amino adipate and 2-amino-4-phosphonobutyrate were studied. Aspartate (10 mM), which is known to eliminate the light response of cells postsynaptic to photoreceptors, induced a marked increase of 150% in the resting efflux of 3H-taurine but did not decrease significantly the light-stimulated release. Tetrodotoxin, which blocks amacrine cell responses, decreased 3H-taurine release stimulated by light by less than 20%. The efflux of taurine was unaffected by strychnine, picrotoxin, tubocurarine, atropine, chlorpromazine, and 2-amino-4-phosphonobutyrate, whereas it was increased by glutamate diethyl esther and alpha-amino adipate. These results, all together, point to photoreceptors as the cells releasing 3H-taurine in response to light.