Evidence map›Paper›PMID 9596790›Full record

ArticleThe Journal of physiology1998

Functional contribution of the alpha5 subunit to neuronal nicotinic channels expressed by chick sympathetic ganglion neurones.

C R Yu, L W Role

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. A novel nicotinic acetylcholine receptor subtype in basal forebrain cholinergic neurons with high sensitivity to amyloid peptides.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Identification of sequence motifs that target neuronal nicotinic receptors to dendrites and axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    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

2 authors at 1 institution in 1 country.

C R YuDepartment of Anatomy and Cell Biology in the Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
L W Role
Columbia University · US

Funding

MODULATORY EFFECTS OF SUBSTANCE P ON AUTONOMIC NEURONSR01NS022061 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI PLOTKIN, JOSHUA L · 1985 to 2019
$9.6M
NINDS NIH HHS NS 22061NINDS NIH HHS R01 NS022061
6 · The paper itself

Abstract

1. Heterologous expression studies of the alpha5 subunit of the neuronal acetylcholine receptor (nAChR) gene family have demonstrated that it can participate in the function of ACh-gated channels if co-expressed with another alpha- and a beta-subunit. Previous studies also indicate prominent expression of alpha5 in both central and peripheral nervous systems. The participation of alpha5 in native nAChRs and its functional role in these channels is, however, unknown. 2. In this study, we present evidence that alpha5 has a role in at least two distinct subtypes of nAChR complexes expressed by embryonic chick sympathetic neurones. 3. alpha5 contributes not only to agonist but also to antagonist sensitivity of natively expressed nAChR channels. Functional deletion of the alpha5 subunit by antisense oligonucleotide treatment removes the nAChRs with relatively low affinity to ACh and cytisine. Deletion of alpha5 also eliminates channels that are blocked by the alpha7-specific antagonist methyllycaconitine (MLA) while increasing the percentage of current carried by nAChRs that are sensitive to alpha-bungarotoxin (alpha-BgTx). 4. Single channel analyses indicate that functional deletion of alpha5 results in the deletion of both the 'brief' and 'long' open duration, 50 pS subtypes of nAChR channels while increasing the expression of the 18 pS, alpha-BgTx-sensitive native nAChRs normally detected in sympathetic neurones at later developmental stages. 5. The biophysical and pharmacological profiles of native nAChRs revealed by this study and previous work are discussed in the context of a proposed model of the nAChR channels expressed by chick sympathetic neurones throughout development.

Indexed as

AcetylcholineAconitineAlkaloidsAnimalsAntisense Elements (Genetics)AzocinesBungarotoxinsChick EmbryoDose-Response Relationship, DrugElectrophysiologyGanglia, SympatheticGene DeletionInsecticidesIon Channel GatingMutagenesisNeuronsAcetylcholineAconitineAlkaloidsAntisense Elements (Genetics)AzocinesBungarotoxinscytisineInsecticidesmethyllycaconitineNicotinic AgonistsNicotinic AntagonistsQuinolizidine AlkaloidsQuinolizinesReceptors, Nicotinic

Identifiers

PMID9596790
PMCPMC2231009
OpenAlexW1970556455

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.