Evidence map›Paper›PMID 21216257›Full record

ReviewNeuropharmacology2011

GABA and central neuropathic pain following spinal cord injury.

Young S Gwak, Claire E Hulsebosch

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 5 pooled it
6.9field-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

105 citing papers in PubMed, 5 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Efficacy of neuromodulation and rehabilitation approaches on pain relief in patients with spinal cord injury: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  19. Ethanolic Extracts ofAdvances in pharmacological and pharmaceutical sciences · 2024
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45 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

2 authors at 1 institution in 1 country.

Young S GwakDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1043, USA. ysgwak@utmb.edu
Claire E Hulsebosch
The University of Texas Medical Branch at Galveston · US

Funding

VISCERAL PAINP01NS011255 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI NEUGEBAUER, VOLKER · 1985 to 2012
$13.6M
CHRONIC CENTRAL PAIN IN SPINAL CORD INJURYP01NS039161 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HULSEBOSCH, CLAIRE E · 2001 to 2005
$5.8M
NINDS NIH HHS NS11255NINDS NIH HHS NS39161NINDS NIH HHS P01 NS011255NINDS NIH HHS P01 NS039161
6 · The paper itself

Abstract

Spinal cord injury induces maladaptive synaptic transmission in the somatosensory system that results in chronic central neuropathic pain. Recent literature suggests that glial-neuronal interactions are important modulators in synaptic transmission following spinal cord injury. Neuronal hyperexcitability is one of the predominant phenomenon caused by maladaptive synaptic transmission via altered glial-neuronal interactions after spinal cord injury. In the somatosensory system, spinal inhibitory neurons counter balance the enhanced synaptic transmission from peripheral input. For a decade, the literature suggests that hypofunction of GABAergic inhibitory tone is an important factor in the enhanced synaptic transmission that often results in neuronal hyperexcitability in dorsal horn neurons following spinal cord injury. Neurons and glial cells synergistically control intracellular chloride ion gradients via modulation of chloride transporters, extracellular glutamate and GABA concentrations via uptake mechanisms. Thus, the intracellular "GABA-glutamate-glutamine cycle" is maintained for normal physiological homeostasis. However, hyperexcitable neurons and glial activation after spinal cord injury disrupts the balance of chloride ions, glutamate and GABA distribution in the spinal dorsal horn and results in chronic neuropathic pain. In this review, we address spinal cord injury induced mechanisms in hypofunction of GABAergic tone that results in chronic central neuropathic pain. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'.

Indexed as

Animalsgamma-Aminobutyric AcidHumansInterneuronsNeuralgiaNeurogliaPosterior Horn CellsSpinal CordSpinal Cord InjuriesSynaptic Transmissiongamma-Aminobutyric Acid

Identifiers

PMID21216257
PMCPMC3285561
OpenAlexW2076919372

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.