Evidence map›Paper›PMID 19029183›Full record

ArticleThe Journal of physiology2009

Postsynaptic action of GABA in modulating sensory transmission in co-cultures of rat carotid body via GABA(A) receptors.

Min Zhang, Katherine Clarke, Huijun Zhong, Cathy Vollmer, Colin A Nurse

Abstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023
    Review
  4. Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    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. Neurotransmitter Modulation of Carotid Body Germinal Niche.International journal of molecular sciences · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Revisiting cAMP signaling in the carotid body.Frontiers in physiology · 2014
    Review
  18. Review
  19. Endogenous H2S is required for hypoxic sensing by carotid body glomus cells.American journal of physiology. Cell physiology · 2012
    Article
  20. Prenatal nicotine exposure increases GABA signaling and mucin expression in airway epithelium.American journal of respiratory cell and molecular biology · 2011
    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

5 authors.

Min ZhangDepartment of Biology, McMaster University, Hamilton, Ontario, Canada.
Katherine Clarke
Huijun Zhong
Cathy Vollmer
Colin A Nurse

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GABA is expressed in carotid body (CB) chemoreceptor type I cells and has previously been reported to modulate sensory transmission via presynaptic GABA(B) receptors. Because low doses of clinically important GABA(A) receptor (GABA(A)R) agonists, e.g. benzodiazepines, have been reported to depress afferent CB responses to hypoxia, we investigated the potential contribution of GABA(A)R in co-cultures of rat type I cells and sensory petrosal neurones (PNs). During gramicidin perforated-patch recordings (to preserve intracellular Cl-), GABA and/or the GABA(A) agonist muscimol (50 microm) induced a bicuculline-sensitive membrane depolarization in isolated PNs. GABA-induced whole-cell currents reversed at approximately -38 mV and had an EC50 of approximately 10 microm (Hill coefficient = approximately 1) at -60 mV. During simultaneous PN and type I cell recordings at functional chemosensory units in co-culture, bicuculline reversibly potentiated the PN, but not type I cell, depolarizing response to hypoxia. Application of the CB excitatory neurotransmitter ATP (1 microm) over the soma of functional PN induced a spike discharge that was markedly suppressed during co-application with GABA (2 microm), even though GABA alone was excitatory. RT-PCR analysis detected expression of GABAergic markers including mRNA for alpha1, alpha2, beta2, gamma2S, gamma2L and gamma3 GABA(A)R subunits in petrosal ganglia extracts. Also, CB extracts contained mRNAs for GABA biosynthetic markers, i.e. glutamate decarboxylase (GAD) isoforms GAD 67A,E, and GABA transporter isoforms GAT 2,3 and BGT-1. In CB sections, sensory nerve endings apposed to type I cells were immunopositive for the GABA(A)R beta subunit. These data suggest that GABA, released from the CB during hypoxia, inhibits sensory discharge postsynaptically via a shunting mechanism involving GABA(A) receptors.

Indexed as

Action PotentialsAdenosine TriphosphateAnimalsCarotid BodyCell HypoxiaCells, CulturedChemoreceptor CellsCoculture TechniquesDose-Response Relationship, DrugGABA AgonistsGABA AntagonistsGABA-A Receptor AgonistsGABA-A Receptor AntagonistsGABA-B Receptor AgonistsGABA-B Receptor AntagonistsGABA Plasma Membrane Transport ProteinsAdenosine TriphosphateGABA AgonistsGABA AntagonistsGABA-A Receptor AgonistsGABA-A Receptor AntagonistsGABA-B Receptor AgonistsGABA-B Receptor AntagonistsGABA Plasma Membrane Transport ProteinsGabrb2 protein, ratgamma-Aminobutyric AcidGlutamate DecarboxylaseReceptors, GABA-AReceptors, GABA-B

Identifiers

PMID19029183
PMCPMC2670048

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.