ArticleThe Journal of physiology2011
Synaptic vesicles control the time course of neurotransmitter secretion via a Ca²+/H+ antiport.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Functionally distinct evoked and spontaneous neurotransmission operate via a shared pool of synaptic vesicles in viscerosensory afferents.The Journal of physiology · 2025Article
- Article
- Association of soil selenium, strontium, and magnesium concentrations with Parkinson's disease mortality rates in the USA.Environmental geochemistry and health · 2018Article
- Ultrafast and Slow Cholinergic Transmission. Different Involvement of Acetylcholinesterase Molecular Forms.Molecules (Basel, Switzerland) · 2017Review
- Activation of a TRP-like channel and intracellular Ca2+ dynamics during phospholipase-C-mediated cell death.Journal of cell science · 2014Article
- Presynaptic K(+) channels, vesicular Ca(2+)/H (+) antiport--synaptotagmin, and acetylcholinesterase, three mechanisms cutting short the cholinergic signal at neuromuscular and nerve-electroplaque junctions.Journal of molecular neuroscience : MN · 2014Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the physiological role of the vesicular Ca2+/H+ antiport in rapid synaptic transmission using the Torpedo electric organ (a modified neuromuscular system). By inhibiting V-type H+-transporting ATPase (V-ATPase), bafilomycin A1 dissipates the H+ gradient of synaptic vesicles, thereby abolishing the Ca2+/H+ antiport driving force. In electrophysiology experiments, bafilomycin A1 significantly prolonged the duration of the evoked electroplaque potential. A biochemical assay for acetylcholine (ACh) release showed that the effect of bafilomycin A1 was presynaptic. Indeed, bafilomycin A1 increased the amount of radio-labelled ACh released in response to paired-pulse stimulation. Bafilomycin A1 also enhanced Ca2+-dependent ACh release from isolated nerve terminals (synaptosomes). The bafilomycin-induced electroplaque potential lengthening did not arise from cholinesterase inhibition, since eserine (which also prolonged the electroplaque potential) strongly decreased evoked ACh release. Bafilomycin A1 augmented the amount of calcium accumulating in nerve terminals following a short tetanic stimulation and delayed subsequent calcium extrusion. By reducing stimulation-dependent calcium accumulation in synaptic vesicles, bafilomycin A1 diminished the corresponding depletion of vesicular ACh, as tested using both intact tissue and isolated synaptic vesicles. Strontium ions inhibit the vesicular Ca2+/H+ antiport, while activating transmitter release at concentrations one order of magnitude higher than Ca2+ does. In the presence of Sr2+ the time course of the electroplaque potential was also prolonged but, unlike bafilomycin A1, Sr2+ enhanced facilitation in paired-pulse experiments. It is therefore proposed that the vesicular Ca2+/H+ antiport function is to shorten 'phasic' transmitter release, allowing the synapse to transmit briefer impulses and so to work at higher frequencies.
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