ArticleProceedings of the National Academy of Sciences of the United States of America2004
Cumulative inactivation of N-type CaV2.2 calcium channels modified by alternative splicing.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Influence of T-Bar on Calcium Concentration Impacting Release Probability.Frontiers in computational neuroscience · 2022Article
- Metabolic insights from a GHSR-A203E mutant mouse model.Molecular metabolism · 2020Article
- Tissue- and cell-specific expression of a splice variant in the II-III cytoplasmic loop of Cacna1b.FEBS open bio · 2019Article
- Four novel interaction partners demonstrate diverse modulatory effects on voltage-gated CaPflugers Archiv : European journal of physiology · 2019Article
- Constitutive activity of the Ghrelin receptor reduces surface expression of voltage-gated CaJournal of cell science · 2017Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Article
- The tetramerization domain potentiates Kv4 channel function by suppressing closed-state inactivation.Biophysical journal · 2014Article
- Alternative splicing: functional diversity among voltage-gated calcium channels and behavioral consequences.Biochimica et biophysica acta · 2013Review
- Systematic mapping of the state dependence of voltage- and Ca2+-dependent inactivation using simple open-channel measurements.The Journal of general physiology · 2010Article
- The inhibition of neuronal calcium ion channels by trace levels of yttrium released from carbon nanotubes.Biomaterials · 2009Article
- Alternative splicing in the synaptic protein interaction site of rat Ca(v)2.2 (alpha (1B)) calcium channels: changes induced by chronic inflammatory pain.Journal of molecular neuroscience : MN · 2009Article
- Differential role of N-type calcium channel splice isoforms in pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Differential regulation of endogenous N- and P/Q-type Ca2+ channel inactivation by Ca2+/calmodulin impacts on their ability to support exocytosis in chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Alternative splicing controls G protein-dependent inhibition of N-type calcium channels in nociceptors.Nature neuroscience · 2007Article
- G-proteins modulate cumulative inactivation of N-type (Cav2.2) calcium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Alternative splicing in the C-terminus of CaV2.2 controls expression and gating of N-type calcium channels.The Journal of physiology · 2006Article
- Neuronal L-type calcium channels open quickly and are inhibited slowly.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Ca(V)2 family of voltage-gated calcium channels, present in presynaptic nerve terminals, regulates exocytosis and synaptic transmission. Cumulative inactivation of these channels occurs during trains of action potentials, and this may control short-term dynamics at the synapse. Inactivation during brief, repetitive stimulation is primarily attributed to closed-state inactivation, and several factors modulate the susceptibility of voltage-gated calcium channels to this form of inactivation. We show that alternative splicing of an exon in a cytoplasmic region of the Ca(V)2.2 channel modulates its sensitivity to inactivation during trains of action potential waveforms. The presence of this exon, exon 18a, protects the Ca(V)2.2 channel from entry into closed-state inactivation specifically during short (10 ms to 3 s) and small depolarizations of the membrane potential (-60 mV to -50 mV). The reduced sensitivity to closed-state inactivation within this dynamic range likely underlies the differential responsiveness of Ca(V)2.2 splice isoforms to trains of action potential waveforms. Regulated alternative splicing of Ca(V)2.2 represents a possible mechanism for modulating short-term dynamics of synaptic efficacy in different regions of the nervous system.
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Registered trials
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.