ArticleNature1989
Membrane depolarization evokes neurotransmitter release in the absence of calcium entry.
Article in Nature, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 91 citations in OpenAlex.
- CaProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Translationally Controlled Tumor Protein Stimulates Dopamine Release from PC12 Cells via CaInternational journal of molecular sciences · 2016Article
- What are the mechanisms for analogue and digital signalling in the brain?Nature reviews. Neuroscience · 2013Review
- Control of neurotransmitter release: From Ca2+ to voltage dependent G-protein coupled receptors.Pflugers Archiv : European journal of physiology · 2010Review
- Historical view and physiology demonstration at the NMJ of the crayfish opener muscle.Journal of visualized experiments : JoVE · 2009Article
- Long-lasting hyperexcitability induced by depolarization in the absence of detectable Ca2+ signals.Journal of neurophysiology · 2009Article
- Analog modulation of mossy fiber transmission is uncoupled from changes in presynaptic Ca2+.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- A simulation study on the Ca2+-independent but voltage-dependent exocytosis and endocytosis in dorsal root ganglion neurons.European biophysics journal : EBJ · 2005Article
- Release of neurotransmitter induced by Ca2+-uncaging: reexamination of the ca-voltage hypothesis for release.Journal of computational neuroscience · 2005Article
- The timing of phasic transmitter release is Ca2+-dependent and lacks a direct influence of presynaptic membrane potential.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Evidence for a voltage-dependent enhancement of neurotransmitter release mediated via the synaptic protein interaction site of N-type Ca2+ channels.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Neurotransmitter release evoked by nerve impulses without Ca2+ entry through Ca2+ channels in frog motor nerve endings.The Journal of physiology · 1995Article
- Neurotransmitter release at fast synapses.The Journal of membrane biology · 1994Review
- Relation of exocytotic release of gamma-aminobutyric acid to Ca2+ entry through Ca2+ channels or by reversal of the Na+/Ca2+ exchanger in synaptosomes.Pflugers Archiv : European journal of physiology · 1993Article
- Spatial facilitation and depression within one motor nerve terminal of frogs.The Journal of physiology · 1993Article
- Effect of an intracellular calcium chelator on the regulation of electrically evoked [3H]-noradrenaline release from rat hippocampal slices.British journal of pharmacology · 1993Article
- Contribution of Ca2+ inflow to quantal, phasic transmitter release from nerve terminals of frog muscle.Pflugers Archiv : European journal of physiology · 1992Article
- Time course of transmitter release calculated from simulations of a calcium diffusion model.Biophysical journal · 1992Article
- Regulation of cytosolic free calcium concentration by intrasynaptic mitochondria.Molecular biology of the cell · 1992Article
- Evoked phasic release in frog nerve terminals obtained after block of Ca2+ entry by Cd2+.Pflugers Archiv : European journal of physiology · 1991Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery that Ca2+ is necessary for the release of neurotransmitter, the primary means by which nerve cells communicate, led to the calcium hypothesis of neutransmitter release, in which release is initiated after an action potential only by an increase in intracellular Ca2+ concentration near the release sites and is terminated (1-2 ms) by the rapid removal of Ca2+. Since then, the calcium-voltage hypothesis has been proposed, in which the depolarization of the presynaptic terminals has two functions. First, in common with the calcium hypothesis, the Ca2+ conductance is increased, thereby permitting Ca2+ entry. Second, a conformational change is induced in a membrane molecule that renders it sensitive to Ca2+, and then binding of Ca2+ to this active form triggers release of neurotransmitter. When the membrane is repolarized, the molecule is inactivated and release is terminated, regardless of the local Ca2+ concentration at that moment. This hypothesis, in contrast to the calcium hypothesis, accounts for the insensitivity of the time course of release to experimental manipulations of intracellular Ca2+ concentration. Furthermore, it explains rapid termination of release after depolarization, even though Ca2+ concentration may still be high. Here we describe experiments that distinguish between these two hypotheses and find that our results support the calcium voltage hypothesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.