Evidence map›Paper›PMID 12601155›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Subtype-selective reconstitution of synaptic transmission in sympathetic ganglion neurons by expression of exogenous calcium channels.

Sumiko Mochida, Ruth E Westenbroek, Charles T Yokoyama, Kanako Itoh, William A Catterall

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Neurotransmitter Release Site Replenishment and Presynaptic Plasticity.International journal of molecular sciences · 2020
    Review
  5. Presynaptic Calcium Channels.International journal of molecular sciences · 2019
    Review
  6. The Role of CaCell reports · 2019
    Article
  7. In vitro and in vivo phosphorylation of the CaChannels (Austin, Tex.) · 2018
    Review
  8. Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  9. The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016
    Review
  10. Article
  11. Article
  12. Exogenous α-synuclein decreases raft partitioning of Cav2.2 channels inducing dopamine release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  13. Review
  14. Article
  15. Calcium channels and short-term synaptic plasticity.The Journal of biological chemistry · 2013
    Review
  16. Article
  17. Fine-tuning synaptic plasticity by modulation of Ca(V)2.1 channels with Ca2+ sensor proteins.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Review
  19. Article
  20. Review
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 2 institutions in 2 countries.

Sumiko MochidaDepartment of Physiology, Tokyo Medical University, Tokyo 160-8402, Japan.
Ruth E Westenbroek
Charles T Yokoyama
Kanako Itoh
William A Catterall
University of Washington · USTokyo Medical University · JP

Funding

MOLECULAR PROPERTIES OF VOLTAGE-SENSITIVE CHANNELSR01NS022625 · NINDS · UNIVERSITY OF WASHINGTON · PI CATTERALL, WILLIAM A · 1985 to 2019
$6.2M
NINDS NIH HHS NS22625NINDS NIH HHS R01 NS022625
6 · The paper itself

Abstract

Fast cholinergic neurotransmission between superior cervical ganglion neurons (SCGNs) in cell culture is initiated by N-type Ca(2+) currents through Ca(v)2.2 channels. To test the ability of different Ca(2+)-channel subtypes to initiate synaptic transmission in these cells, SCGNs were injected with cDNAs encoding Ca(v)1.2 channels, which conduct L-type currents, Ca(v)2.1 channels, which conduct P/Q-type Ca(2+) currents, and Ca(v)2.3 channels, which conduct R-type Ca(2+) currents. Exogenously expressed Ca(v)2.1 channels were localized in nerve terminals, as assessed by immunocytochemistry with subtype-specific antibodies, and these channels effectively initiated synaptic transmission. Injection with cDNA encoding Ca(v)2.3 channels yielded a lower level of presynaptic labeling and synaptic transmission, whereas injection with cDNA encoding Ca(v)1.2 channels resulted in no presynaptic labeling and no synaptic transmission. Our results show that exogenously expressed Ca(2+) channels can mediate synaptic transmission in SCGNs and that the specificity of reconstitution of neurotransmission (Ca(v)2.1 > Ca(v)2.3 >> Ca(v)1.2) follows the same order as in neurons in vivo. The specificity of reconstitution of neurotransmission parallels the specificity of trafficking of these Ca(v) channels to nerve terminals.

Indexed as

Cation Transport ProteinsAgatoxinsAnimalsBrainCalciumCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, R-TypeCells, CulturedDNA, ComplementaryGanglia, SympatheticGlutathione TransferaseImmunohistochemistryNeuronsPatch-Clamp TechniquesRatsAgatoxinsCacna1e protein, ratCalciumCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, R-TypeCation Transport ProteinsDNA, ComplementaryGlutathione Transferaseomega-agatoxin IRecombinant Fusion ProteinsSpider Venoms

Identifiers

PMID12601155
PMCPMC151423
OpenAlexW2075030357

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.