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C Hull, H VonGersdorff; High Intracellular Chloride Concentrations Modulate the Rate of Synaptic Vesicle Endocytosis in Bipolar Cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1946.
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Purpose: To date, no neurotransmitter has been implicated as a modulator of synaptic vesicle endocytosis. Here, we used measurements of membrane capacitance to show that elevated intracellular chloride mediated by ionotropic GABA receptors dramatically alters the kinetics of endocytosis presynaptically at the Mb1 type bipolar cell terminal in goldfish retina. Methods: Whole-cell and perforated patch clamp recordings were performed on isolated presynaptic terminals in both acutely dissociated and in situ bipolar cells from the retina of goldfish. High time-resolution membrane capacitance measurements were used as an assay of synaptic vesicle endocytosis. Results: In acutely dissociated terminals, dialyzing chloride into the terminal via patch pipette slowed the kinetics of endocytosis in a dose-dependent manner, with complete inhibition of endocytosis occurring at 125 mM Cl-. In addition, presynaptic terminals in situ subject to spontaneous and/or evoked GABA/glycinergic input showed much slower kinetics of endocytosis. In these terminals, endocytosis was accelerated by blocking presynaptic chloride influx with picrotoxin and strychnine. Similarly, local application of GABA to acutely dissociated synaptic terminals led to a profound reduction in the kinetics of endocytosis. Conclusion: These preliminary results suggest that GABA and glycine can act as presynaptic modulators of the rate of synaptic vesicle endocytosis at this synapse.
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