ArticleProceedings of the National Academy of Sciences of the United States of America2003
The timing of phasic transmitter release is Ca2+-dependent and lacks a direct influence of presynaptic membrane potential.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. 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, 53 citations in OpenAlex.
- Enhanced Release Probability without Changes in Synaptic Delay during Analogue-Digital Facilitation.Cells · 2024Article
- CaEMBO reports · 2022Article
- Autocrine inhibition by a glutamate-gated chloride channel mediates presynaptic homeostatic depression.Science advances · 2021Article
- CaProceedings of the National Academy of Sciences of the United States of America · 2019Article
- An Exclusion Zone for Ca2+ Channels around Docked Vesicles Explains Release Control by Multiple Channels at a CNS Synapse.PLoS computational biology · 2015Article
- Nanodomain coupling explains Ca²⁺ independence of transmitter release time course at a fast central synapse.eLife · 2014Article
- Axonal noise as a source of synaptic variability.PLoS computational biology · 2014Article
- What are the mechanisms for analogue and digital signalling in the brain?Nature reviews. Neuroscience · 2013Review
- A novel fast mechanism for GPCR-mediated signal transduction--control of neurotransmitter release.The Journal of cell biology · 2011Article
- Vesicle pools: lessons from adrenal chromaffin cells.Frontiers in synaptic neuroscience · 2011Article
- Control of neurotransmitter release: From Ca2+ to voltage dependent G-protein coupled receptors.Pflugers Archiv : European journal of physiology · 2010Review
- Developmental regulation of the intracellular Ca2+ sensitivity of vesicle fusion and Ca2+-secretion coupling at the rat calyx of Held.The Journal of physiology · 2009Article
- Action potential modulates Ca2+-dependent and Ca2+-independent secretion in a sensory neuron.Biophysical journal · 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
- Interactions between multiple sources of short-term plasticity during evoked and spontaneous activity at the rat calyx of Held.The Journal of physiology · 2008Article
- Dopamine inhibits basal prolactin release in pituitary lactotrophs through pertussis toxin-sensitive and -insensitive signaling pathways.Endocrinology · 2008Article
- A mechanism intrinsic to the vesicle fusion machinery determines fast and slow transmitter release at a large CNS synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Scotopic visual signaling in the mouse retina is modulated by high-affinity plasma membrane calcium extrusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Physiological temperatures reduce the rate of vesicle pool depletion and short-term depression via an acceleration of vesicle recruitment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Rapid vesicular release, quantal variability, and spillover contribute to the precision and reliability of transmission at a glomerular synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ influx through voltage-gated Ca2+ channels and the resulting elevation of intracellular Ca2+ concentration, [Ca2+]i, triggers transmitter release in nerve terminals. However, it is controversial whether in addition to the opening of Ca2+ channels, membrane potential directly affects transmitter release. Here, we assayed the influence of membrane potential on transmitter release at the calyx of Held nerve terminals. Transmitter release was evoked by presynaptic Ca2+ uncaging, or by presynaptic Ca2+ uncaging paired with presynaptic voltage-clamp depolarizations to +80 mV, under pharmacological block of voltage-gated Ca2+ channels. Such a change in membrane potential did not alter the Ca2+ dependence of transmitter release rates or synaptic delays. We also found, by varying the amount of Ca2+ influx during Ca2+ tail-currents, that the time course of phasic transmitter release is not invariant to changes in release probability. Rather, the time difference between peak Ca2+ current and peak transmitter release became progressively shorter with increasing Ca2+ current amplitude. When this time difference was plotted as a function of the estimated local [Ca2+]i at the sites of vesicle fusion, a slope of approximately 100 micros per 10 microM [Ca2+]i was found, in reasonable agreement with a model of cooperative Ca2+ binding and vesicle fusion. Thus, the amplitude and time course of the [Ca2+]i signal at the sites of vesicle fusion controls the timing and the amount of transmitter release, both under conditions of brief periods of Ca2+ influx, as well as during step-like elevations of [Ca2+]i produced by Ca2+ uncaging.
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