Evidence map›Paper›PMID 19498419›Full record

ArticleActa pharmacologica Sinica2009

Cross-regulation between colocalized nicotinic acetylcholine and 5-HT3 serotonin receptors on presynaptic nerve terminals.

John J Dougherty, Robert A Nichols

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Serotonin ReceptorInternational journal of environmental research and public health · 2022
    Article
  2. Article
  3. Review
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  10. Rehabilitating a brain with Alzheimer's: a proposal.Clinical interventions in aging · 2011
    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

2 authors at 2 institutions in 1 country.

John J DoughertyDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Robert A Nichols
Drexel University · USUniversity of Hawaiʻi at Mānoa · US

Funding

Beta Amyloid and Presynaptic Nicotinic ReceptorsR01AG021586 · NIA · UNIVERSITY OF HAWAII AT MANOA · PI NICHOLS, ROBERT ALAN · 2004 to 2007
$887k
NIA NIH HHS AG 21586NIA NIH HHS R01 AG021586
6 · The paper itself

Abstract

aimSubstantial colocalization of functionally independent alpha4 nicotinic acetylcholine receptors and 5-HT(3) serotonin receptors on presynaptic terminals has been observed in brain. The present study was aimed at addressing whether nicotinic acetylcholine receptors and 5-HT(3) serotonin receptors interact on the same presynaptic terminal, suggesting a convergence of cholinergic and serotonergic regulation.

methodsCa(2+) responses in individual, isolated nerve endings purified from rat striatum were measured using confocal imaging.

resultsApplication of 500 nmol/L nicotine following sustained stimulation with the highly selective 5-HT(3) receptor agonist m-chlorophenylbiguanide at 100 nmol/L resulted in markedly reduced Ca(2+) responses (28% of control) in only those striatal nerve endings that originally responded to m-chlorophenylbiguanide. The cross-regulation developed over several minutes. Presynaptic nerve endings that had not responded to m-chlorophenylbiguanide, indicating that 5-HT(3) receptors were not present, displayed typical responses to nicotine. Application of m-chlorophenylbiguanide following sustained stimulation with nicotine resulted in partially attenuated Ca(2+) responses (49% of control). Application of m-chlorophenylbiguanide following sustained stimulation with m-chlorophenylbiguanide also resulted in a strong attenuation of Ca(2+) responses (12% of control), whereas nicotine-induced Ca(2+) responses following sustained stimulation with nicotine were not significantly different from control.

conclusionThese results indicate that the presynaptic Ca(2+) increases evoked by either 5-HT(3) receptor or nicotinic acetylcholine receptor activation regulate subsequent responses to 5-HT(3) receptor activation, but that only 5-HT(3) receptors cross-regulate subsequent nicotinic acetylcholine receptor-mediated responses. The findings suggest a specific interaction between the two receptor systems in the same striatal nerve terminal, likely involving Ca(2+)-dependent intracellular pathways that regulate these signaling systems at one or more levels.

Indexed as

AnimalsBiguanidesCalciumCorpus StriatumMaleMicroscopy, ConfocalNicotineNicotinic AgonistsPresynaptic TerminalsRatsRats, Sprague-DawleyReceptors, NicotinicReceptors, Serotonin, 5-HT3Serotonin Receptor AgonistsSignal Transduction1-(3-chlorophenyl)biguanideBiguanidesCalciumNicotineNicotinic AgonistsReceptors, NicotinicReceptors, Serotonin, 5-HT3Serotonin Receptor Agonists

Identifiers

PMID19498419
PMCPMC4002366
OpenAlexW1989041710

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.