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Activation of the Tonic GABA_C Receptor Current in Retinal Bipolar Cell Terminals by Nonvesicular GABA Release

Neuroscience Group, Institute for Science and Technology in Medicine, Keele University, Keele, United Kingdom

Submitted 1 April 2009; accepted in final form 1 June 2009

Within the second synaptic layer of the retina, bipolar cell (BC) output to ganglion cells is regulated by inhibitory input to BC axon terminals. GABA_A receptors (GABA_ARs) mediate rapid synaptic currents in BC terminals, whereas GABA_C receptors (GABA_CRs) mediate slow evoked currents and a tonic current, which is strongly regulated by GAT-1 GABA transporters. We have used voltage-clamp recordings from BC terminals in goldfish retinal slices to determine the source of GABA for activation of these currents. Inhibition of vesicular release with concanamycin A or tetanus toxin significantly inhibited GABA_AR inhibitory postsynaptic currents and glutamate-evoked GABA_AR and GABA_CR currents but did not reduce the tonic GABA_CR current, which was also not dependent on extracellular Ca²⁺. The tonic current was strongly potentiated by inhibition of GABA transaminase, under both normal and Ca²⁺-free conditions, and was activated by exogenous taurine; however inhibition of taurine transport had little effect. The tonic current was unaffected by GAT-2/3 inhibition and was potentiated by GAT-1 inhibition even in the absence of vesicular release, indicating that it is unlikely to be evoked by reversal of GABA transporters or by ambient GABA. In addition, GABA release does not appear to occur via hemichannels or P2X₇ receptors. BC terminals therefore exhibit two forms of GABA_CR-mediated inhibition, activated by vesicular and by nonvesicular GABA release, which are likely to have distinct functions in visual signal processing. The tonic GABA_CR current in BC terminals exhibits similar properties to tonic GABA_AR and glutamate receptor currents in the brain.