GABA release by dopaminergic amacrine (DA) cells of the mouse retina was detected by measuring Cl^- currents generated by isolated perikarya in response to their own neurotransmitter. The possibility that the Cl^- currents were caused by GABA release from synaptic endings that had survived the dissociation of the retina was ruled out by examining confocal Z series of the surface of dissociated tyrosine hydroxylase-positive perikarya after staining with antibodies to pre- and postsynaptic markers. GABA release was caused by exocytosis because (i) the current events were transient on the millisecond time scale and thus resembled miniature synaptic currents; (ii) they were abolished by treatment with a blocker of the vesicular proton pump, bafilomycin A1; (iii) their frequency was controlled by the intracellular Ca²⁺ concentration. Since DA cells' perikarya do not contain presynaptic active zones, release was by necessity extrasynaptic. A range of depolarizing stimuli caused GABA exocytosis, showing that extrasynaptic release of GABA is controlled by DA cells' electrical activity. With all modalities of stimulation, including long-lasting square pulses, segments of pacemaker activity delivered by the action-potential-clamp method and high frequency trains of ramps, discharge of GABAergic currents exhibited considerable variability in latency and duration, suggesting that coupling between Ca²⁺ influx and transmitter exocytosis is extremely loose in comparison with the synapse. Paracrine signaling based on extrasynaptic release of GABA by DA cells and other GABAergic amacrines may participate in controlling the excitability of the neuronal processes that interact synaptically in the inner plexiform layer.