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

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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; τ > 10 s) were significantly slower than those in acutely dissociated terminals (double exponential decay; τfast ≅ 1-2 s; τslow > 10 s). Surprisingly, GABAA and/or GABAC 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 Ca2+ buffer. These results suggest a new role for GABA and Cl- ions in blocking the trigger for fast endocytosis at this ribbon-type synapse.

Original languageEnglish (US)
Pages (from-to)469-482
Number of pages14
Issue number3
Publication statusPublished - Oct 28 2004


ASJC Scopus subject areas

  • Neuroscience(all)

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