ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Ca2+ from one or two channels controls fusion of a single vesicle at the frog neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Cellular and synaptic specializations for sub-millisecond precision in the mammalian auditory brainstem.Frontiers in cellular neuroscience · 2025Review
- Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024Review
- Spontaneous neurotransmission at evocable synapses predicts their responsiveness to action potentials.Frontiers in cellular neuroscience · 2023Article
- Single Calcium Channel Nanodomains Drive Presynaptic Calcium Entry at Lamprey Reticulospinal Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Microphysiological Modeling of the Structure and Function of Neuromuscular Transmitter Release Sites.Frontiers in synaptic neuroscience · 2022Review
- Dynamics of Neuromuscular Transmission Reproduced by Calcium-Dependent and Reversible Serial Transitions in the Vesicle Fusion Complex.Frontiers in synaptic neuroscience · 2021Article
- Rapid regulation of vesicle priming explains synaptic facilitation despite heterogeneous vesicle:CaeLife · 2020Article
- Nanomachinery Organizing Release at Neuronal and Ribbon Synapses.International journal of molecular sciences · 2019Review
- Presynaptic mechanisms controlling calcium-triggered transmitter release at the neuromuscular junction.Current opinion in physiology · 2018Article
- Article
- Transmitter release site organization can predict synaptic function at the neuromuscular junction.Journal of neurophysiology · 2018Article
- Calcium dependence of spontaneous neurotransmitter release.Journal of neuroscience research · 2018Review
- Lambert-Eaton myasthenic syndrome: mouse passive-transfer model illuminates disease pathology and facilitates testing therapeutic leads.Annals of the New York Academy of Sciences · 2018Review
- Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction.Journal of visualized experiments : JoVE · 2017Article
- Transmitter release is evoked with low probability predominately by calcium flux through single channel openings at the frog neuromuscular junction.Journal of neurophysiology · 2015Article
- New insights into short-term synaptic facilitation at the frog neuromuscular junction.Journal of neurophysiology · 2015Article
- Single calcium channel domain gating of synaptic vesicle fusion at fast synapses; analysis by graphic modeling.Channels (Austin, Tex.) · 2015Article
- Global Ca2+ signaling drives ribbon-independent synaptic transmission at rod bipolar cell synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Estimation of presynaptic calcium currents and endogenous calcium buffers at the frog neuromuscular junction with two different calcium fluorescent dyes.Frontiers in synaptic neuroscience · 2014Article
- Synaptic vesicle tethering and the CaV2.2 distal C-terminal.Frontiers in cellular neuroscience · 2014Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotransmitter release is triggered by the cooperative action of approximately five Ca2+ ions entering the presynaptic terminal through Ca2+ channels. Depending on the organization of the active zone (AZ), influx through one or many channels may be needed to cause fusion of a vesicle. Using a combination of experiments and modeling, we examined the number of channels that contribute Ca2+ for fusion of a single vesicle in a frog neuromuscular AZ. We compared Ca2+ influx to neurotransmitter release by measuring presynaptic action potential-evoked (AP-evoked) Ca2+ transients simultaneously with postsynaptic potentials. Ca2+ influx was manipulated by changing extracellular [Ca2+] (Ca(ext)) to alter the flux per channel or by reducing the number of open Ca2+ channels with omega-conotoxin GVIA (omega-CTX). When Ca(ext) was reduced, the exponent of the power relationship relating release to Ca2+ influx was 4.16 +/- 0.62 (SD; n = 4), consistent with a biochemical cooperativity of approximately 5. In contrast, reducing influx with omega-CTX yielded a power relationship of 1.7 +/- 0.44 (n = 5) for Ca(ext) of 1.8 mM and 2.12 +/- 0.44 for Ca(ext) of 0.45 mM (n = 5). Using geometrically realistic Monte Carlo simulations, we tracked Ca2+ ions as they entered through each channel and diffused in the terminal. Experimental and modeling data were consistent with two to six channel openings per AZ per AP; the Ca2+ that causes fusion of a single vesicle originates from one or two channels. Channel cooperativity depends mainly on the physical relationship between channels and vesicles and is insensitive to changes in the non-geometrical parameters of our model.
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