Evidence map›Paper›PMID 9826733›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Evidence for a voltage-dependent enhancement of neurotransmitter release mediated via the synaptic protein interaction site of N-type Ca2+ channels.

S Mochida, C T Yokoyama, D K Kim, K Itoh, W A Catterall

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Biophysical model of muscle spindle encoding.Experimental physiology · 2024
    Review
  4. Review
  5. CaProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. GABAThe Journal of physiology · 2019
    Article
  7. Review
  8. Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  9. Article
  10. Article
  11. Review
  12. Trafficking and stability of voltage-gated calcium channels.Cellular and molecular life sciences : CMLS · 2012
    Review
  13. KIF5B motor adaptor syntabulin maintains synaptic transmission in sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  14. Article
  15. K+ channel facilitation of exocytosis by dynamic interaction with syntaxin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

S MochidaDepartment of Physiology, Tokyo Medical College, Tokyo 160, Japan.
C T Yokoyama
D K Kim
K Itoh
W A Catterall
Neurological Surgery · USUniversity of Washington · USTokyo Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secretion of neurotransmitters is initiated by voltage-gated calcium influx through presynaptic, voltage-gated N-type calcium channels. These channels interact with the SNARE proteins, which are core components of the exocytosis process, via the synaptic protein interaction (synprint) site in the intracellular loop connecting domains II and III of their alpha1B subunit. Interruption of this interaction by competing synprint peptides inhibits fast, synchronous transmitter release. Here we identify a voltage-dependent, but calcium-independent, enhancement of transmitter release that is elicited by trains of action potentials in the presence of a hyperosmotic extracellular concentration of sucrose. This enhancement of transmitter release requires interaction of SNARE proteins with the synprint site. Our results provide evidence for a voltage-dependent signal that is transmitted by protein-protein interactions from the N-type calcium channel to the SNARE proteins and enhances neurotransmitter release by altering SNARE protein function.

Indexed as

Vesicular Transport ProteinsAction PotentialsAnimalsCalcium ChannelsEgtazic AcidExcitatory Postsynaptic PotentialsExocytosisMembrane ProteinsNerve Tissue ProteinsNeuronsNeurotransmitter AgentsPeptidesRatsSNARE ProteinsSuperior Cervical GanglionSynapses1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCalcium ChannelsEgtazic AcidMembrane ProteinsNerve Tissue ProteinsNeurotransmitter AgentsPeptidesSNARE ProteinsVesicular Transport Proteins

Identifiers

PMID9826733
PMCPMC24406
OpenAlexW2035585669

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.