Evidence map›Paper›PMID 26415765›Full record

ArticleNeuroscience2015

Inflammatory mediator-induced modulation of GABAA currents in human sensory neurons.

X-L Zhang, K-Y Lee, B T Priest, I Belfer, M S Gold

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. OnabotulinumtoxinA effects on trigeminal nociceptors.Cephalalgia : an international journal of headache · 2023
    Article
  9. Article
  10. Pre-Synaptic GABACells · 2022
    Article
  11. Review
  12. Studying human nociceptors: from fundamentals to clinic.Brain : a journal of neurology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Human Dorsal Root Ganglia.Frontiers in cellular neuroscience · 2019
    Review
  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

5 authors at 2 institutions in 1 country.

X-L ZhangDepartment of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
K-Y LeeDepartment of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
B T PriestLilly Research Laboratories, Indianapolis, IN 46285, USA.
I BelferDepartment of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
M S GoldDepartment of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; Pittsburgh Center for Pain Research, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: msg22@pitt.edu.
University of Pittsburgh · USEli Lilly (United States) · US

Funding

Inflammation-induced changes in spinal GABA-A receptor signalingR01NS063010 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOLD, MICHAEL S · 2009 to 2011
$1.1M
NINDS NIH HHS 1R01NS063010NINDS NIH HHS R01 NS063010
6 · The paper itself

Abstract

The purpose of the present study was to characterize the properties of A-type GABA receptor (GABAA receptor) currents in human sensory neurons. Neurons were obtained from adult organ donors. GABAA currents were recorded in isolated neurons. Both large inactivating low-affinity currents and smaller persistent high-affinity currents were present in all of the 129 neurons studied from 15 donors. The kinetics of human GABAA currents were slower than those in rat sensory neurons. GABA currents were completely blocked by bicuculline (10 μM), and persistent currents were activated by the δ-subunit-preferring agonist, 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridine-3-ol (THIP). The GABA current equilibrium potential was ∼ 20 mV more hyperpolarized than in rat neurons. Both low- and high-affinity currents were increased by inflammatory mediators but via different second messenger pathways. These results highlight potentially important species differences in the properties of ion channels present in their native environment and suggest the use of human sensory neurons may be a valuable tool to test compounds prior to use in humans.

Indexed as

AdultFemaleGABA-A Receptor Agonistsgamma-Aminobutyric AcidGanglia, SpinalHumansInflammation MediatorsMaleMembrane PotentialsMiddle AgedReceptors, GABA-ASensory Receptor CellsGABA-A Receptor Agonistsgamma-Aminobutyric AcidInflammation MediatorsReceptors, GABA-Adorsal root ganglionintracellular Cl(−) concentrationpatch clampprotein kinase Aprotein kinase Ctyrosine kinase

Identifiers

PMID26415765
PMCPMC4633346
OpenAlexW2205156358

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.