Evidence map›Paper›PMID 18936079›Full record

ArticleThe Journal of physiology2008

Spontaneous purinergic neurotransmission in the mouse urinary bladder.

John S Young, En Meng, Tom C Cunnane, Keith L Brain

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2008. 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
2.6field-weighted citation impact, top 12% 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, 49 citations in OpenAlex.

  1. Review
  2. Article
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  4. Regulation of P2X1 receptors by modulators of the cAMP effectors PKA and EPAC.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Review
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  8. Electrophysiology of Syncytial Smooth Muscle.Journal of experimental neuroscience · 2019
    Review
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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

4 authors at 3 institutions in 3 countries.

John S YoungDepartment of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK. john.s.young@gmail.com
En Meng
Tom C Cunnane
Keith L Brain
University of Oxford · GBMansfield University · USTri-Service General Hospital · TW

Funding

Wellcome Trust 069768Wellcome Trust 074128
6 · The paper itself

Abstract

Spontaneous purinergic neurotransmission was characterized in the mouse urinary bladder, a model for the pathological or ageing human bladder. Intracellular electrophysiological recording from smooth muscle cells of the detrusor muscle revealed spontaneous depolarizations, distinguishable from spontaneous action potentials (sAPs) by their amplitude (< 40 mV) and insensitivity to the L-type Ca(2+) channel blocker nifedipine (1 microm) (100 +/- 29%). Spontaneous depolarizations were abolished by the P2X(1) receptor antagonist NF449 (10 microm) (frequency 8.5 +/- 8.5% of controls), insensitive to the muscarinic acetylcholine receptor antagonist atropine (1 microm) (103.4 +/- 3.0%), and became more frequent in latrotoxin (LTX; 1 nm) (438 +/- 95%), suggesting that they are spontaneous excitatory junction potentials (sEJPs). Such sEJPs were correlated, in amplitude and timing, with focal Ca(2+) transients in smooth muscle cells (measured using confocal microscopy), suggesting a common origin: ATP binding to P2X(1) receptors. sAPs were abolished by NF449, insensitive to atropine (126 +/- 39%) and increased in frequency by LTX (930 +/- 450%) suggesting a neurogenic, purinergic origin, in common with sEJPs. By comparing the kinetics of sAPs and sEJPs, we demonstrated that sAPs occur when sufficient cation influx through P2X(1) receptors triggers L-type Ca(2+) channels; the first peak of the differentiated rising phase of depolarizations - attributed to the influx of cations through the P2X(1) receptor - is of larger amplitude for sAPs (2248 mV s(-1)) than sEJPs (439 mV s(-1)). Surprisingly, sAPs in the mouse urinary bladder, unlike those from other species, are triggered by stochastic ATP release from parasympathetic nerve terminals rather than being myogenic.

Indexed as

Action PotentialsAdenosine TriphosphateAnimalsAtropineBenzenesulfonatesCalcium Channel BlockersCalcium Channels, L-TypeCalcium SignalingFemaleKineticsMaleMembrane PotentialsMiceMice, Inbred C57BLMyocytes, Smooth MuscleNeurotransmitter Agents4,4,',4'',4'''-(carbonylbis(imino-5,1,3-benzenetriylbis(carbonylimino)))tetrakis(benzene-1,3-disulfonate)Adenosine Triphosphatealpha-latrotoxinAtropineBenzenesulfonatesCalcium Channel BlockersCalcium Channels, L-TypeNeurotransmitter AgentsNifedipinePurinergic P2 Receptor AgonistsPurinergic P2 Receptor AntagonistsReceptors, PurinergicReceptors, Purinergic P2XSpider Venoms

Identifiers

PMID18936079
PMCPMC2655397
OpenAlexW2095937483

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.