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The Journal of Neuroscience, June 28, 2006, 26(26):6979-6984; doi:10.1523/JNEUROSCI.1386-06.2006

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Brief Communications
GABA Transporters Regulate a Standing GABA_C Receptor-Mediated Current at a Retinal Presynaptic Terminal

Court Hull, Geng-Lin Li, and Henrique von Gersdorff

The Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239

Correspondence should be addressed to Dr. Henrique von Gersdorff, The Vollum Institute, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239. Email: vongersd{at}ohsu.edu

At the axon terminal of goldfish retinal bipolar cells, GABA_C receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABA_C receptors. 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 GABA_C receptors. We propose that this GABA_C receptor-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 GABA_C receptor-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) GABA_C current implicates them in a novel role as major determinants of presynaptic excitability.

Key words: bipolar cell; retina; GAT-1; GABA transporters; tonic inhibition; presynaptic excitability

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Received March 31, 2006; revised May 15, 2006; accepted May 22, 2006.

Correspondence should be addressed to Dr. Henrique von Gersdorff, The Vollum Institute, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239. Email: vongersd{at}ohsu.edu

This article has been cited by other articles:

				S. M. Jones and M. J. Palmer Activation of the Tonic GABAC Receptor Current in Retinal Bipolar Cell Terminals by Nonvesicular GABA Release J Neurophysiol, August 1, 2009; 102(2): 691 - 699. [Abstract] [Full Text] [PDF]

				S. H. Mørkve and E. Hartveit Properties of glycine receptors underlying synaptic currents in presynaptic axon terminals of rod bipolar cells in the rat retina J. Physiol., August 1, 2009; 587(15): 3813 - 3830. [Abstract] [Full Text] [PDF]

				H. Hirasawa, M. Puopolo, and E. Raviola Extrasynaptic Release of GABA by Retinal Dopaminergic Neurons J Neurophysiol, July 1, 2009; 102(1): 146 - 158. [Abstract] [Full Text] [PDF]

				L. Oltedal, M. L. Veruki, and E. Hartveit Passive membrane properties and electrotonic signal processing in retinal rod bipolar cells J. Physiol., February 15, 2009; 587(4): 829 - 849. [Abstract] [Full Text] [PDF]

				G.-L. Li, J. Vigh, and H. von Gersdorff Short-Term Depression at the Reciprocal Synapses between a Retinal Bipolar Cell Terminal and Amacrine Cells J. Neurosci., July 11, 2007; 27(28): 7377 - 7385. [Abstract] [Full Text] [PDF]

				M. J. Palmer Functional segregation of synaptic GABAA and GABAC receptors in goldfish bipolar cell terminals J. Physiol., November 15, 2006; 577(1): 45 - 53. [Abstract] [Full Text] [PDF]

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