Evidence map›Paper›PMID 19494193›Full record

ArticleJournal of neurophysiology2009

Activation of the tonic GABAC receptor current in retinal bipolar cell terminals by nonvesicular GABA release.

S M Jones, M J Palmer

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Dopamine-Dependent Sensitization of Rod Bipolar Cells by GABA Is Conveyed through Wide-Field Amacrine Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  3. Article
  4. Article
  5. GABAρ subunits confer a bicuculline-insensitive component to GFAP+ cells of cerebellum.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Allosteric modulation of retinal GABA receptors by ascorbic acid.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  16. Article
  17. An Update on GABAρ Receptors.Current neuropharmacology · 2010
    Article
  18. 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

2 authors at 1 institution in 1 country.

S M JonesNeuroscience Group, Institute for Science and Technology in Medicine, Keele University, Keele, Staffordshire ST5 5BG, United Kingdom.
M J Palmer
Keele University · GB

Funding

Medical Research Council G0800502
6 · The paper itself

Abstract

Within the second synaptic layer of the retina, bipolar cell (BC) output to ganglion cells is regulated by inhibitory input to BC axon terminals. GABA(A) receptors (GABA(A)Rs) mediate rapid synaptic currents in BC terminals, whereas GABA(C) receptors (GABA(C)Rs) mediate slow evoked currents and a tonic current, which is strongly regulated by GAT-1 GABA transporters. We have used voltage-clamp recordings from BC terminals in goldfish retinal slices to determine the source of GABA for activation of these currents. Inhibition of vesicular release with concanamycin A or tetanus toxin significantly inhibited GABA(A)R inhibitory postsynaptic currents and glutamate-evoked GABA(A)R and GABA(C)R currents but did not reduce the tonic GABA(C)R current, which was also not dependent on extracellular Ca(2+). The tonic current was strongly potentiated by inhibition of GABA transaminase, under both normal and Ca(2+)-free conditions, and was activated by exogenous taurine; however inhibition of taurine transport had little effect. The tonic current was unaffected by GAT-2/3 inhibition and was potentiated by GAT-1 inhibition even in the absence of vesicular release, indicating that it is unlikely to be evoked by reversal of GABA transporters or by ambient GABA. In addition, GABA release does not appear to occur via hemichannels or P2X(7) receptors. BC terminals therefore exhibit two forms of GABA(C)R-mediated inhibition, activated by vesicular and by nonvesicular GABA release, which are likely to have distinct functions in visual signal processing. The tonic GABA(C)R current in BC terminals exhibits similar properties to tonic GABA(A)R and glutamate receptor currents in the brain.

Indexed as

4-Aminobutyrate TransaminaseAnimalsCalciumExocytosisGABA Plasma Membrane Transport ProteinsGABA Uptake Inhibitorsgamma-Aminobutyric AcidGlutamic AcidGoldfishInhibitory Postsynaptic PotentialsIn Vitro TechniquesMembrane PotentialsPatch-Clamp TechniquesPurinergic P2 Receptor AntagonistsReceptors, GABAReceptors, GABA-A4-Aminobutyrate TransaminaseCalciumGABA-C receptorGABA Plasma Membrane Transport ProteinsGABA Uptake Inhibitorsgamma-Aminobutyric AcidGlutamic AcidPurinergic P2 Receptor AntagonistsReceptors, GABAReceptors, GABA-AReceptors, Purinergic P2Receptors, Purinergic P2X7

Identifiers

PMID19494193
PMCPMC2724346
OpenAlexW2039885274

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.