GABA transporters regulate a standing GABAC receptor-mediated current at a retinal presynaptic terminal.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Hull, C; Li, G-L; von Gersdorff, H

Published Date

  • June 28, 2006

Published In

Volume / Issue

  • 26 / 26

Start / End Page

  • 6979 - 6984

PubMed ID

  • 16807327

Pubmed Central ID

  • PMC3572852

Electronic International Standard Serial Number (EISSN)

  • 1529-2401

Digital Object Identifier (DOI)

  • 10.1523/JNEUROSCI.1386-06.2006


  • eng

Conference Location

  • United States