Evidence map›Paper›PMID 15760934›Full record

ArticleThe Journal of physiology2005

Ca2+ permeability of nicotinic acetylcholine receptors from rat dorsal root ganglion neurones.

Sergio Fucile, Antonietta Sucapane, Fabrizio Eusebi

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The Role of TRP Channels in Nicotinic Provoked Pain and Irritation from the Oral Cavity and Throat: Translating Animal Data to Humans.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Review
  5. Article
  6. Sensory Effects of Nicotine and Tobacco.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Nicotinic acetylcholine receptors in dorsal root ganglion neurons include the α6β4* subtype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    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

3 authors at 1 institution in 1 country.

Sergio FucileIstituto Pasteur Fondazione Cenci-Bolognetti and Dipartimento di Fisiologia Umana e Farmacologia, Centro di Eccellenza Biologia e Medicina Molecolare, Università di Roma La Sapienza, Roma, Italy. sergio.fucile@uniroma1.it
Antonietta Sucapane
Fabrizio Eusebi
Istituto Pasteur · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca2+ entry through neuronal nicotinic ACh receptors (nAChRs) modulates many biological processes in nervous tissue. In order to study the functional role of nAChRs in peripheral sensory signalling, we measured their Ca2+ permeability in rat dorsal root ganglion (DRG) neurones, and analysed the effects of nAChR-mediated Ca2+ influx on the function of the vanilloid receptor TRPV1. The fractional Ca2+ current (P(f), i.e. the percentage of current carried by Ca2+ ions) flowing through nAChR channels was measured by Ca2+ imaging fluorescence microscopy in combination with the patch-clamp technique. Functional nAChRs were expressed in a subset of adult DRG neurones (about 24% of the cells), typically with small to medium size as measured by their capacitance (40 +/- 3 pF). In most cells, ACh evoked slowly desensitizing currents, insensitive to methyllycaconitine (MLA, 10 nm), a potent antagonist of homomeric nAChRs. Fast decaying currents, probably mediated by alpha7*-nAChRs (i.e. native alpha7-containing nAChRs), were observed in 15% of ACh-responsive cells, in which slowly decaying currents, mediated by heteromeric nAChRs, were simultaneously present. The nAChRs of adult DRG neurones exhibited a P(f) value of 2.2 +/- 0.6% in the presence of MLA and 1.9 +/- 0.6% (P > 0.1) in the absence of MLA, indicating that homomeric MLA-sensitive nAChRs do not contribute to Ca2+ entry into adult DRG neurones. Conversely, 10% of neonatal DRG neurones showed ACh-evoked currents completely blocked by MLA. In these neurones, nAChRs showed a larger P(f) value (9.5 +/- 1.5%), indicating the expression of bona fide alpha7*-nAChRs. Finally, we report that Ca2+ influx through nAChRs in adult DRG neurones negatively modulated the TRPV1-mediated responses, representing a possible mechanism underlying the analgesic properties of nicotinic agonists on sensory neurones.

Indexed as

AnimalsCalciumCalcium SignalingCapsaicinCell Membrane PermeabilityCells, CulturedGanglia, SpinalIon Channel GatingIon ChannelsMembrane PotentialsNeuronsNicotineRatsRats, WistarReceptors, NicotinicTRPV Cation ChannelsCalciumCapsaicinIon ChannelsNicotineReceptors, NicotinicTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID15760934
PMCPMC1464485
OpenAlexW2151798397

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.