GABA Transporters Regulate a Standing GABACReceptor-Mediated Current at a Retinal Presynaptic Terminal

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Abstract
At the axon terminal of goldfish retinal bipolar cells, GABACreceptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABACreceptors. Selective inhibition of GAT-1 GABA transporters on amacrine cells increases this tonic current and reveals a specific functional coupling between GAT-1 transporters and GABACreceptors. We propose that this GABACreceptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABACreceptor-mediated reciprocal feedback between bipolar cell terminals and amacrine cells is greatly increased when GAT-1 transporters are specifically blocked by NO-711 (1-[2-[[(diphenylmethylene)imino]oxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride). The involvement of GAT-1 transporters in regulating this standing (or tonic) GABACcurrent implicates them in a novel role as major determinants of presynaptic excitability.