GABA transporters regulate a standing GABAC receptor-mediated current at a retinal presynaptic terminal.
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.
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Related Subject Headings
- Retinal Bipolar Cells
- Retina
- Receptors, GABA
- Presynaptic Terminals
- Neurology & Neurosurgery
- In Vitro Techniques
- Goldfish
- GABA Uptake Inhibitors
- GABA Plasma Membrane Transport Proteins
- Electrophysiology
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Retinal Bipolar Cells
- Retina
- Receptors, GABA
- Presynaptic Terminals
- Neurology & Neurosurgery
- In Vitro Techniques
- Goldfish
- GABA Uptake Inhibitors
- GABA Plasma Membrane Transport Proteins
- Electrophysiology