The characteristics and ionic dependence of the release of [3H]gamma-aminobutyric acid ([3H]GABA) and [3H]taurine from the chick retina, stimulated by kainic acid (KA) and by depolarizing concentrations of potassium was examined and compared to those of [3H]dopamine. KA (100 microM) highly stimulated the release of [3H]GABA (25-fold over resting efflux), induced a moderate increase in [3H]taurine and did not increase the efflux of [3H]dopamine. The efflux of [3H]GABA stimulated by KA was totally calcium-independent but it was markedly sodium and chloride dependent. Chloride dependence was assessed by replacing chloride with the impermeant anion gluconate, or by addition of the anion transport blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Depolarizing concentrations of KCl (56 mM) stimulated the release of [3H]GABA, [3H]taurine and [3H]dopamine to about the same extent. The release of [3H]GABA and [3H]taurine was only partially calcium dependent, in contrast to the highly calcium-dependent efflux of [3H]dopamine. A sodium-free medium increased the resting efflux and decreased the potassium-stimulated release of [3H]GABA and [3H]taurine; the resting efflux of [3H]dopamine was unaffected and the potassium-induced efflux was somewhat increased. The potassium-stimulated efflux of [3H]GABA and [3H]taurine showed a chloride-dependent component which was higher for taurine whereas the resting efflux was not modified. The stimulated release of [3H]dopamine was increased in a chloride-free medium. The ionic dependence of KA and potassium stimulated efflux of [3H]GABA and [3H]taurine showed properties similar to those of the homoexchange-activated efflux of amino acids which was also found sodium and chloride dependent and clearly different from the calcium-coupled neurotransmitter release process. Exposure of retinas to KA and potassium produced retinal cell swelling which is prevented in a chloride-free medium. Results are discussed in terms of a particular efflux mechanism for [3H]GABA and [3H]taurine in the retina in response to stimulation associated with changes in ionic gradients and retinal cell swelling.