ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Syntaxin modulation of calcium channels in cortical synaptosomes as revealed by botulinum toxin C1.
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 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 66 citations in OpenAlex.
- Early and transient increase in cortical pyramidal cell excitability and delayed alteration of evoked synaptic transmission and t-SNARE proteins content in the hippocampus and neocortex of neonatal and juvenileFrontiers in cellular neuroscience · 2026Article
- Neurons require glucose uptake and glycolysis in vivo.Cell reports · 2023Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
- 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
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Syntaxin requirement for Ca2+-triggered exocytosis in neurons and endocrine cells demonstrated with an engineered neurotoxin.Biochemistry · 2011Article
- Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells.Toxins · 2010Review
- A mutation in the first intracellular loop of CACNA1A prevents P/Q channel modulation by SNARE proteins and lowers exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Calcium-sensing receptor activation depresses synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Direct interaction of endogenous Kv channels with syntaxin enhances exocytosis by neuroendocrine cells.PloS one · 2008Article
- Gamma-band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- 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
- 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
- Targeted mutations in the syntaxin H3 domain specifically disrupt SNARE complex function in synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Direct interaction of a brain voltage-gated K+ channel with syntaxin 1A: functional impact on channel gating.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- SNARE proteins contribute to calcium cooperativity of synaptic transmission.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Molecular determinants of the functional interaction between syntaxin and N-type Ca2+ channel gating.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Syntaxin modulation of slow inactivation of N-type calcium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Presynaptic frequency- and pattern-dependent filtering.Journal of computational neuroscienceReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When the presynaptic membrane protein syntaxin is coexpressed in Xenopus oocytes with N- or P/Q-type Ca(2+) channels, it promotes their inactivation (Bezprozvanny et al., 1995; Wiser et al., 1996, 1999; Degtiar et al., 2000) (I. B. Bezprozvanny, P. Zhong, R. H. Scheller, and R. W. Tsien, unpublished observations). These findings led to the hypothesis that syntaxin influences Ca(2+) channel function in presynaptic endings, in a reversal of the conventional flow of information from Ca(2+) channels to the release machinery. We examined this effect in isolated mammalian nerve terminals (synaptosomes). Botulinum neurotoxin type C1 (BoNtC1), which cleaves syntaxin, was applied to rat neocortical synaptosomes at concentrations that completely blocked neurotransmitter release. This treatment altered the pattern of Ca(2+) entry monitored with fura-2. Whereas the initial Ca(2+) rise induced by depolarization with K(+)-rich solution was unchanged, late Ca(2+) entry was strongly augmented by syntaxin cleavage. Similar results were obtained when Ca(2+) influx arose from repetitive firing induced by the K(+)-channel blocker 4-aminopyridine. Cleavage of vesicle-associated membrane protein with BoNtD or SNAP-25 with BoNtE failed to produce a significant change in Ca(2+) entry. The BoNtC1-induced alteration in Ca(2+) signaling was specific to voltage-gated Ca(2+) channels, not Ca(2+) extrusion or buffering, and it involved N-, P/Q- and R-type channels, the high voltage-activated channels most intimately associated with presynaptic release machinery. The modulatory effect of syntaxin was not immediately manifest when synaptosomes had been K(+)-predepolarized in the absence of external Ca(2+), but developed with a delay after admission of Ca(2+), suggesting that vesicular turnover may be necessary to make syntaxin available for its stabilizing effect on Ca(2+) channel inactivation.
Indexed as
Identifiers
10844005PMC6772436W2137533720What 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.