Evidence map›Paper›PMID 22733659›Full record

ArticleThe Journal of physiology2012

P2Y2 receptor activation opens pannexin-1 channels in rat carotid body type II cells: potential role in amplifying the neurotransmitter ATP.

Min Zhang, Nikol A Piskuric, Cathy Vollmer, Colin A Nurse

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

51 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Therapeutic potential for P2YPurinergic signalling · 2023
    Review
  9. Review
  10. Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023
    Review
  11. Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  12. The Carotid Body "Tripartite Synapse": Role of Gliotransmission.Advances in experimental medicine and biology · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022
    Review
  17. Neurotransmitter Modulation of Carotid Body Germinal Niche.International journal of molecular sciences · 2020
    Review
  18. Review
  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

4 authors at 1 institution in 1 country.

Min ZhangDepartment of Biology, McMaster University, 1280 Main St. West, Hamilton, Ontario L8S 4K1, Canada.
Nikol A Piskuric
Cathy Vollmer
Colin A Nurse
McMaster University · CA

Funding

Canadian Institutes of Health Research MOP 12037
6 · The paper itself

Abstract

Signal processing in the carotid body (CB) is initiated at receptor glomus (or type I) cells which depolarize and release the excitatory neurotransmitter ATP during chemoexcitation by hypoxia and acid hypercapnia. Glomus cell clusters (GCs) occur in intimate association with glia-like type II cells which express purinergic P2Y2 receptors (P2Y2Rs) but their function is unclear. Here we immunolocalize the gap junction-like protein channel pannexin-1 (Panx-1) in type II cells and show Panx-1 mRNA expression in the rat CB. As expected, type II cell activation within or near isolated GCs by P2Y2R agonists, ATP and UTP (100 μm), induced a rise in intracellular [Ca(2+)]. Moreover in perforated-patch whole cell recordings from type II cells, these agonists caused a prolonged depolarization and a concentration-dependent, delayed opening of non-selective ion channels that was prevented by Panx-1 blockers, carbenoxolone (5 μm) and 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS; 10 μm). Because Panx-1 channels serve as conduits for ATP release, we hypothesized that paracrine, type II cell P2Y2R activation leads to ATP-induced ATP release. In proof-of-principle experiments we used co-cultured chemoafferent petrosal neurones (PNs), which express P2X2/3 purinoceptors, as sensitive biosensors of ATP released from type II cells. In several cases, UTP activation of type II cells within or near GCs led to depolarization or increased firing in nearby PNs, and the effect was reversibly abolished by the selective P2X2/3 receptor blocker, pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10 μm). We propose that CB type II cells may function as ATP amplifiers during chemotransduction via paracrine activation of P2Y2Rs and Panx-1 channels.

Indexed as

Adenosine TriphosphateAnimalsCalciumCarotid BodyCells, CulturedConnexinsElectrophysiological PhenomenaGene ExpressionMembrane PotentialsModels, NeurologicalNerve Tissue ProteinsNeurotransmitter AgentsParacrine CommunicationRatsReceptors, Purinergic P2Y2RNA, MessengerAdenosine TriphosphateCalciumConnexinsNerve Tissue ProteinsNeurotransmitter Agentspannexin 1, ratReceptors, Purinergic P2Y2RNA, Messenger

Identifiers

PMID22733659
PMCPMC3473289
OpenAlexW1523526154

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.