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J Physiol Volume 556, Number 2, 347-352, April 15, 2004 DOI: 10.1113/jphysiol.2003.058818
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RAPID REPORT

Hydrogen ions control synaptic vesicle ion channel activity in Torpedo electromotor neurones

Ronit Ahdut-Hacohen1, Dessislava Duridanova2, Halina Meiri1 and Rami Rahamimoff1

1 Department of Physiology and the Bernard Katz Minerva Centre for Cell Biophysics, The Hebrew University- Hadassah Medical School, Jerusalem 91120, Israel2 Institute for Biophysics, The Bulgarian Academy of Sciences, Sofia, Bulgaria

During exocytosis the synaptic vesicle fuses with the surface membrane and undergoes a pH jump. When the synaptic vesicle is inside the presynaptic nerve terminal its internal pH is about 5.5 and after fusion, the inside of the vesicle comes in contact with the extracellular medium with a pH of about 7.25. We examined the effect of such pH jump on the opening of the non-specific ion channel in the synaptic vesicle membrane, in the context of the post-fusion hypothesis of transmitter release control. The vesicles were isolated from Torpedo ocellata electromotor neurones. The pH dependence of the opening of the non-specific ion channel was examined using the fused vesicle-attached configuration of the patch clamp technique. The rate of opening depends on both pH and voltage. Increasing the pH from 5.5 to 7.25 activated dramatically the non-specific ion channel of the vesicle membrane. The single channel conductance did not change significantly with the alteration in the pH, and neither did the mean channel open time. These results support the hypothesis that during partial fusion of the vesicle with the surface membrane, ion channels in the vesicle membrane open, admit ions and thus help in the ion exchange process mechanism, leading to the release of the transmitter from the intravesicular ion exchange matrix. This process may have also a pathophysiological significance in conditions of altered pH.

(Received 27 November 2003; accepted after revision 13 February 2004; first published online 20 February 2004)
Corresponding author R. Rahamimoff: Department of Physiology and the Bernard Katz Minerva Centre for Cell Biophysics, The Hebrew University–Hadassah Medical School, Jerusalem 91120, Israel. Email: ramir{at}cc.huji.ac.il




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