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

Court Hull, Geng Lin Li, Henrique Von Gersdorff

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

At the axon terminal of goldfish retinal bipolar cells, GABAC receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABAC 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 GABAC receptors. We propose that this GABAC receptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca 2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABAC 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) GABAC current implicates them in a novel role as major determinants of presynaptic excitability.

Original languageEnglish (US)
Pages (from-to)6979-6984
Number of pages6
JournalJournal of Neuroscience
Volume26
Issue number26
DOIs
StatePublished - 2006

Fingerprint

GABA Plasma Membrane Transport Proteins
Presynaptic Terminals
Amacrine Cells
Retinal Bipolar Cells
Goldfish
Niacin
gamma-Aminobutyric Acid
Action Potentials
GABA-C receptor

Keywords

  • Bipolar cell
  • Gaba transporters
  • GAT-1
  • Presynaptic excitability
  • Retina
  • Tonic inhibition

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

GABA transporters regulate a standing GABAC receptor-mediated current at a retinal presynaptic terminal. / Hull, Court; Li, Geng Lin; Von Gersdorff, Henrique.

In: Journal of Neuroscience, Vol. 26, No. 26, 2006, p. 6979-6984.

Research output: Contribution to journalArticle

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abstract = "At the axon terminal of goldfish retinal bipolar cells, GABAC receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABAC 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 GABAC receptors. We propose that this GABAC receptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca 2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABAC 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) GABAC current implicates them in a novel role as major determinants of presynaptic excitability.",
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N2 - At the axon terminal of goldfish retinal bipolar cells, GABAC receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABAC 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 GABAC receptors. We propose that this GABAC receptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca 2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABAC 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) GABAC current implicates them in a novel role as major determinants of presynaptic excitability.

AB - At the axon terminal of goldfish retinal bipolar cells, GABAC receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABAC 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 GABAC receptors. We propose that this GABAC receptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca 2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABAC 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) GABAC current implicates them in a novel role as major determinants of presynaptic excitability.

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