Evidence map›Paper›PMID 12949228›Full record

ArticleThe Journal of physiology2003

GABA mediates autoreceptor feedback inhibition in the rat carotid body via presynaptic GABAB receptors and TASK-1.

Ian M Fearon, Min Zhang, Cathy Vollmer, Colin A Nurse

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

22 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023
    Review
  3. Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  4. Article
  5. Article
  6. Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing.Pflugers Archiv : European journal of physiology · 2015
    Review
  14. Role of K₂p channels in stimulus-secretion coupling.Pflugers Archiv : European journal of physiology · 2015
    Review
  15. Review
  16. Revisiting cAMP signaling in the carotid body.Frontiers in physiology · 2014
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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.

Ian M FearonDepartment of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4K1, Canada. fearoni@mcmaster.ca
Min Zhang
Cathy Vollmer
Colin A Nurse
McMaster University · CA

Funding

Wellcome Trust
6 · The paper itself

Abstract

Background K+ channels exert control over neuronal excitability by regulating resting potential and input resistance. Here, we show that GABAB receptor-mediated activation of a background K+ conductance modulates transmission at rat carotid body chemosensory synapses in vitro. Carotid body chemoreceptor (type I) cells expressed GABAB(1) and GABAB(2) subunits as well as endogenous GABA. The GABAB receptor agonist baclofen activated an anandamide- and Ba2+-sensitive TASK-1-like background K+ conductance in chemoreceptor cell clusters, but was without effect on voltage-gated Ca2+ channels. Hydroxysaclofen (50 microM), 5-aminovaleric acid (100 microM) and CGP 55845 (100 nM), selective GABAB receptor blockers, potentiated the hypoxia-induced receptor potential; this effect was abolished by pre-treatment with pertussis toxin (PTX; 500 ng ml-1), an inhibitor of Gi, or by H-89 (50 microM), a selective inhibitor of protein kinase A. The protein kinase C inhibitor chelerythrine chloride (100 microM) was without effect on this potentiation. GABAB receptor blockers also caused depolarisation of type I cells in clusters, and enhanced spike discharge in spontaneously firing cells. In functional co-cultures of type I clusters and petrosal sensory neurones, GABAB receptor blockers potentiated hypoxia-induced postsynaptic chemosensory responses mediated by the fast-acting transmitters ACh and ATP. Thus GABAB receptor-mediated activation of TASK-1 or a related channel provides a presynaptic autoregulatory feedback mechanism that modulates fast synaptic transmission in the rat carotid body.

Indexed as

Potassium Channels, Tandem Pore DomainAnimalsAutoreceptorsBaclofenCalcium ChannelsCarotid BodyCells, CulturedCyclic AMP-Dependent Protein KinasesElectrophysiologyFeedback, PhysiologicalFluorescent Antibody TechniqueGABA AntagonistsGABA-B Receptor Antagonistsgamma-Aminobutyric AcidMembrane PotentialsNerve Tissue ProteinsAutoreceptorsBaclofenCalcium ChannelsCyclic AMP-Dependent Protein KinasesGABA AntagonistsGABA-B Receptor Antagonistsgamma-Aminobutyric AcidNerve Tissue ProteinsPotassiumPotassium ChannelsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3Receptors, GABA-BReceptors, G-Protein-CoupledReceptors, Presynaptic

Identifiers

PMID12949228
PMCPMC2343478
OpenAlexW2070711857

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.