ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Similar intracellular Ca2+ requirements for inactivation and facilitation of voltage-gated Ca2+ channels in a glutamatergic mammalian nerve terminal.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 19 citations in OpenAlex.
- Interpretation of presynaptic phenotypes of synaptic plasticity in terms of a two-step priming process.The Journal of general physiology · 2024Article
- What calcium channels remember.eLife · 2023Article
- Apparent calcium dependence of vesicle recruitment.The Journal of physiology · 2018Article
- Dynamics of volume-averaged intracellular CaThe Journal of physiology · 2017Article
- Bilirubin augments CaScientific reports · 2017Article
- Neurotransmitter Release Can Be Stabilized by a Mechanism That Prevents Voltage Changes Near the End of Action Potentials from Affecting Calcium Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Large Ca²⁺-dependent facilitation of Ca(V)2.1 channels revealed by Ca²⁺ photo-uncaging.The Journal of physiology · 2015Article
- Ca2+ channel to synaptic vesicle distance accounts for the readily releasable pool kinetics at a functionally mature auditory synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Calcium-buffering effects of gluconate and nucleotides, as determined by a novel fluorimetric titration method.The Journal of physiology · 2014Article
- Synaptic gain-of-function effects of mutant Cav2.1 channels in a mouse model of familial hemiplegic migraine are due to increased basal [Ca2+]i.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Ca2+ channel nanodomains boost local Ca2+ amplitude.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Sustaining rapid vesicular release at active zones: potential roles for vesicle tethering.Trends in neurosciences · 2013Review
- Calretinin regulates Ca2+-dependent inactivation and facilitation of Ca(v)2.1 Ca2+ channels through a direct interaction with the α12.1 subunit.The Journal of biological chemistry · 2012Article
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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
Voltage-gated Ca2+ channels (VGCCs) of the P/Q-type, which are expressed at a majority of mammalian nerve terminals, show two types of Ca2+-dependent feedback regulation-inactivation (CDI) and facilitation (CDF). Because of the nonlinear relationship between Ca2+ influx and transmitter release, CDI and CDF are powerful regulators of synaptic strength. To what extent VGCCs inactivate or facilitate during spike trains depends on the dynamics of free Ca2+ ([Ca2+]i) and the Ca2+ sensitivity of CDI and CDF, which has not been determined in nerve terminals. In this report, we took advantage of the large size of a rat auditory glutamatergic synapse--the calyx of Held--and combined voltage-clamp recordings of presynaptic Ca2+ currents (ICa(V)) with UV-light flash-induced Ca2+ uncaging and presynaptic Ca2+ imaging to study the Ca2+ requirements for CDI and CDF. We find that nearly half of the presynaptic VGCCs inactivate during 100 ms voltage steps and require several seconds to recover. This inactivation is caused neither by depletion of Ca2+ ions from the synaptic cleft nor by metabotropic feedback inhibition, because it is resistant to blockade of metabotropic and ionotropic glutamate receptors. Facilitation of ICa(V) induced by repetitive depolarizations or preconditioning voltage steps decays within tens of milliseconds. Since Ca2+ buffers only weakly affect CDI and CDF, we conclude that the Ca2+ sensors are closely associated with the channel. CDI and CDF can be induced by intracellular photo release of Ca2+ resulting in [Ca2+]i elevations in the low micromolar range, implying a surprisingly high affinity of the Ca2+ sensors.
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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.