Evidence map›Paper›PMID 24641084›Full record

ArticleBritish journal of pharmacology2014

Oxytocin inhibits the activity of acid-sensing ion channels through the vasopressin, V1A receptor in primary sensory neurons.

Fang Qiu, Chun-Yu Qiu, Huilan Cai, Ting-Ting Liu, Zu-Wei Qu, Zhifan Yang, Jia-Da Li, Qun-Yong Zhou, Wang-Ping Hu

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. 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
10.0field-weighted citation impact, top 2% 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, 67 citations in OpenAlex.

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  13. Influence of gap junctions upon CaBiophysics and physicobiology · 2022
    Article
  14. Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019
    Review
  19. Review
  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

9 authors at 3 institutions in 2 countries.

Fang QiuDepartment of Pharmacology, Hubei University of Science and Technology, Xianning, China; College of Life Sciences, Hubei University, Wuhan, China.
Chun-Yu Qiu
Huilan Cai
Ting-Ting Liu
Zu-Wei Qu
Zhifan Yang
Jia-Da Li
Qun-Yong Zhou
Wang-Ping Hu
Hubei University of Science and Technology · CNHubei University · CNUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeA growing number of studies have demonstrated that oxytocin (OT) plays an analgesic role in modulation of nociception and pain. Most work to date has focused on the central mechanisms of OT analgesia, but little is known about whether peripheral mechanisms are also involved. Acid-sensing ion channels (ASICs) are distributed in peripheral sensory neurons and participate in nociception. Here, we investigated the effects of OT on the activity of ASICs in dorsal root ganglion (DRG) neurons. EXPERIMENTAL APPROACH: Electrophysiological experiments were performed on neurons from rat DRG. Nociceptive behaviour was induced by acetic acid in rats and mice lacking vasopressin, V1A receptors. KEY

resultsOT inhibited the functional activity of native ASICs. Firstly, OT dose-dependently decreased the amplitude of ASIC currents in DRG neurons. Secondly, OT inhibition of ASIC currents was mimicked by arginine vasopressin (AVP) and completely blocked by the V1A receptor antagonist SR49059, but not by the OT receptor antagonist L-368899. Thirdly, OT altered acidosis-evoked membrane excitability of DRG neurons and significantly decreased the amplitude of the depolarization and number of action potentials induced by acid stimuli. Finally, peripherally administered OT or AVP inhibited nociceptive responses to intraplantar injection of acetic acid in rats. Both OT and AVP also induced an analgesic effect on acidosis-evoked pain in wild-type mice, but not in V1A receptor knockout mice. CONCLUSIONS AND IMPLICATIONS: These results reveal a novel peripheral mechanism for the analgesic effect of OT involving the modulation of native ASICs in primary sensory neurons mediated by V1A receptors.

Indexed as

Acetic AcidAcid Sensing Ion Channel BlockersAcid Sensing Ion ChannelsAction PotentialsAnalgesicsAnimalsDisease Models, AnimalDose-Response Relationship, DrugFemaleGanglia, SpinalMice, Inbred C57BLMice, KnockoutNociceptionNociceptive PainOxytocinRats, Sprague-DawleyAcetic AcidAcid Sensing Ion Channel BlockersAcid Sensing Ion ChannelsAnalgesicsOxytocinReceptors, VasopressinV1a vasopressin receptor, ratacid-sensing ion channeldorsal root ganglion neuronelectrophysiologyoxytocinpainproton-gated currentV1A receptorvasopressin

Identifiers

PMID24641084
PMCPMC4055206
OpenAlexW1540241568

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.