Evidence map›Paper›PMID 21632935›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Presynaptic alpha2-GABAA receptors in primary afferent depolarization and spinal pain control.

Robert Witschi, Pradeep Punnakkal, Jolly Paul, Jean-Sébastien Walczak, Fernando Cervero, Jean-Marc Fritschy, Rohini Kuner, Ruth Keist, Uwe Rudolph, Hanns Ulrich Zeilhofer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
7.3field-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

65 citing papers in PubMed, 113 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Mechanism-based nonopioid analgesic targets.The Journal of clinical investigation · 2025
    Review
  5. Review
  6. γ1 GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  7. GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. GABABrain structure & function · 2022
    Article
  12. Article
  13. Article
  14. α2-containing γ-aminobutyric acid type A receptors promote stress resiliency in male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  15. The role of spinal cord extrasynaptic αPhysiological reports · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 4 countries.

Robert WitschiInstitute of Pharmacology and Toxicology, University of Zurich, CH-8057 Zurich, Switzerland.
Pradeep Punnakkal
Jolly Paul
Jean-Sébastien Walczak
Fernando Cervero
Jean-Marc Fritschy
Rohini Kuner
Ruth Keist
Uwe Rudolph
Hanns Ulrich Zeilhofer
University of Zurich · CHMcGill University · CAHarvard University · USHeidelberg University · DE

Funding

CIHR DOP-73908European Research Council 250128
6 · The paper itself

Abstract

Spinal dorsal horn GABA(A) receptors are found both postsynaptically on central neurons and presynaptically on axons and/or terminals of primary sensory neurons, where they mediate primary afferent depolarization (PAD) and presynaptic inhibition. Both phenomena have been studied extensively on a cellular level, but their role in sensory processing in vivo has remained elusive, due to inherent difficulties to selectively interfere with presynaptic receptors. Here, we address the contribution of a major subpopulation of GABA(A) receptors (those containing the α2 subunit) to spinal pain control in mice lacking α2-GABA(A) receptors specifically in primary nociceptors (sns-α2(-/-) mice). sns-α2(-/-) mice exhibited GABA(A) receptor currents and dorsal root potentials of normal amplitude in vitro, and normal response thresholds to thermal and mechanical stimulation in vivo, and developed normal inflammatory and neuropathic pain sensitization. However, the positive allosteric GABA(A) receptor modulator diazepam (DZP) had almost completely lost its potentiating effect on PAD and presynaptic inhibition in vitro and a major part of its spinal antihyperalgesic action against inflammatory hyperalgesia in vivo. Our results thus show that part of the antihyperalgesic action of spinally applied DZP occurs through facilitated activation of GABA(A) receptors residing on primary nociceptors.

Indexed as

AnimalsDiazepamGene Expression RegulationHyperalgesiaInjections, SpinalMembrane PotentialsMiceMice, KnockoutMice, TransgenicNeuralgiaNeurons, AfferentNociceptorsPatch-Clamp TechniquesReceptors, GABA-AReceptors, PresynapticSpinal Nerve RootsDiazepamReceptors, GABA-AReceptors, Presynaptic

Identifiers

PMID21632935
PMCPMC3567284
OpenAlexW2073030228

What OpenQuestion holds

Textmetadata
LicenceTDM
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.