ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Syntaxin modulation of slow inactivation of N-type calcium channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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Who cites it
31 citing papers in PubMed, 81 citations in OpenAlex.
- Assessing the Potential of NGF-Differentiated PC12 Cells as a Model for Synaptic Transmission.Molecular neurobiology · 2025Article
- Cross talk between β subunits, intracellular CaPhysiological reports · 2018Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Article
- Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Intra-membrane signaling between the voltage-gated Ca2+-channel and cysteine residues of syntaxin 1A coordinates synchronous release.Scientific reports · 2013Article
- Impairment of catecholamine systems during induction of long-term potentiation at hippocampal CA1 synapses in HPC-1/syntaxin 1A knock-out mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells.Toxins · 2010Review
- Differences in biophysical properties of nucleus accumbens medium spiny neurons emerging from inactivation of inward rectifying potassium currents.Journal of computational neuroscience · 2009Article
- SNAREs: cogs and coordinators in signaling and development.Plant physiology · 2008Review
- Bidirectional modulation of transmitter release by calcium channel/syntaxin interactions in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Analysis of knock-out mice to determine the role of HPC-1/syntaxin 1A in expressing synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- SNAP-29-mediated modulation of synaptic transmission in cultured hippocampal neurons.The Journal of biological chemistry · 2005Article
- Syntaxin 1A regulation of weakly inactivating N-type Ca2+ channels.The Journal of physiology · 2004Article
- Regulation of syntaxin1A-munc18 complex for SNARE pairing in HEK293 cells.The Journal of physiology · 2004Article
- A syntaxin 1, Galpha(o), and N-type calcium channel complex at a presynaptic nerve terminal: analysis by quantitative immunocolocalization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Cumulative inactivation of N-type CaV2.2 calcium channels modified by alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Overexpressed Ca(v)beta3 inhibits N-type (Cav2.2) calcium channel currents through a hyperpolarizing shift of ultra-slow and closed-state inactivation.The Journal of general physiology · 2004Article
- Calcium channels: unanswered questions.Journal of bioenergetics and biomembranes · 2003Review
Corrections and comments
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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
Syntaxin, a membrane protein vital in triggering vesicle fusion, interacts with voltage-gated N- and P/Q-type Ca(2+) channels. This biochemical association is proposed to colocalize Ca(2+) channels and presynaptic release sites, thus supporting rapid and efficient initiation of neurotransmitter release. The syntaxin channel interaction may also support a novel signaling function, to modulate Ca(2+) channels according to the state of the associated release machinery (Bezprozvanny et al., 1995; Wiser et al., 1996; see also Mastrogiacomo et al., 1994). Here we report that syntaxin 1A (syn1A) coexpressed with N-type channels in Xenopus oocytes greatly promoted slow inactivation gating, but had little or no effect on the onset of and recovery from fast inactivation. Accordingly, the effectiveness of syntaxin depended strongly on voltage protocol. Slow inactivation was found for N-type channels even in the absence of syntaxin and could be distinguished from fast inactivation on the basis of its slow kinetics, distinct voltage dependence (voltage-independent at potentials higher than the level of half-inactivation), and temperature independence (Q(10), approximately 0.8). Trains of action potential-like stimuli were more effective than steady depolarizations in stabilizing the slowly inactivated condition. Agents that stimulate protein kinase C decreased the inhibitory effect of syntaxin on N-type channels. Application of BoNtC1 to cleave syntaxin sharply attenuated the modulatory effects on Ca(2+) channel gating, consistent with structural analysis of syntaxin modulation, supporting use of this toxin to test for the impact of syntaxin on Ca(2+) influx in nerve terminals.
Indexed as
Identifiers
10844004PMC6772443W2136956832What OpenQuestion holds
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.