Evidence map›Paper›PMID 12871824›Full record

ReviewBritish journal of pharmacology2003

Modulation of neuronal nicotinic receptor function by the neuropeptides CGRP and substance P on autonomic nerve cells.

Silvia Di Angelantonio, Rashid Giniatullin, Valeria Costa, Elena Sokolova, Andrea Nistri

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Acetylcholine nicotinic receptor subtypes in chromaffin cells.Pflugers Archiv : European journal of physiology · 2018
    Review
  9. Article
  10. Review
  11. The role of anti-CGRP antibodies in the pathophysiology of primary headaches.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. CGRP receptor antagonism and migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2010
    Review
  18. Article
  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 1 country.

Silvia Di AngelantonioBiophysics Sector and INFM Unit, International School for Advanced Studies (SISSA), Via Beirut 4, 34014 Trieste, Italy.
Rashid Giniatullin
Valeria Costa
Elena Sokolova
Andrea Nistri
Scuola Internazionale Superiore di Studi Avanzati · ITFondazione Santa Lucia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. One classical example of how neuropeptides can affect the function of ligand-gated receptors is the modulation of neuronal nicotinic receptors (nAChRs) by substance P. The present review updates current understanding of this action by substance P and compares it with other neuropeptides more recently found to modulate nAChRs in the autonomic nervous system. 2. Calcitonin gene-related peptide (CGRP) and its N-terminal fragments have been shown to exert complex inhibitory as well facilitatory actions on nAChRs. Fragments such as CGRP(1-4), CGRP(1-5) and CGRP(1-6) rapidly and reversibly enhance agonist sensitivity of nAChRs without directly activating those receptors. Longer fragments or the full-length peptide potently inhibit responses mediated by nAChRs via an apparently competitive-type antagonism. This phenomenon differs from the substance P-induced block, which is agonist use-dependent and preferential towards large nicotinic responses. 3. It is argued that the full-length peptides CGRP and substance P might play distinct roles in the activity-dependent modulation of cholinergic neurotransmission, by inhibiting background noise in the case of CGRP or by reducing excessive excitation in the case of substance P. Hence, multiple neuropeptide mechanisms may represent a wide array of fine-tuning processes to regulate nicotinic synaptic transmission. 4. The availability of novel CGRP derivatives with a strong enhancing action on nAChRs may offer new leads for the drug design targeted for potentiation of nAChRs in the autonomic nervous system as well as in the brain, a subject of interest to counteract the deficit of the nAChR function associated with neurodegenerative diseases like Alzheimer's and Parkinson's diseases.

Indexed as

AnimalsAutonomic PathwaysCalcitonin Gene-Related PeptideHumansMembrane PotentialsReceptors, NicotinicSubstance PCalcitonin Gene-Related PeptideReceptors, NicotinicSubstance P

Identifiers

PMID12871824
PMCPMC1573932
OpenAlexW2063435515

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.