Fast endocytosis is inhibited by GABA-mediated chloride influx at a presynaptic terminal.

Journal Article (Journal Article)

Although multiple kinetic components of synaptic vesicle endocytosis have been identified, it has remained unclear whether neurons can differentially modulate these components. Using membrane capacitance measurements from isolated goldfish bipolar cell terminals, we found that the kinetics of endocytosis in retinal slices (single exponential decay; tau > 10 s) were significantly slower than those in acutely dissociated terminals (double exponential decay; tau(fast) approximately 1-2 s; tau(slow) > 10 s). Surprisingly, GABA(A) and/or GABA(C) receptor antagonists restored the fast component of endocytosis to terminals in retinal slices. Blocking GABAergic feedback from reciprocal synapses or removing external Cl(-) ions also allowed for fast endocytosis. Elevating internal Cl(-) via the patch pipette invariably slowed endocytosis, even in terminals dialyzed with increased Ca(2+) buffer. These results suggest a new role for GABA and Cl(-) ions in blocking the trigger for fast endocytosis at this ribbon-type synapse.

Full Text

Duke Authors

Cited Authors

  • Hull, C; von Gersdorff, H

Published Date

  • October 28, 2004

Published In

Volume / Issue

  • 44 / 3

Start / End Page

  • 469 - 482

PubMed ID

  • 15504327

Pubmed Central ID

  • PMC3572843

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/j.neuron.2004.10.010


  • eng

Conference Location

  • United States