Evidence map›Paper›PMID 29847798›Full record

ArticleCell reports2018

NMDA Receptor Activation Underlies the Loss of Spinal Dorsal Horn Neurons and the Transition to Persistent Pain after Peripheral Nerve Injury.

Perrine Inquimbert, Martin Moll, Alban Latremoliere, Chi-Kun Tong, John Whang, Gregory F Sheehan, Brendan M Smith, Erica Korb, Maria C P Athié, Olusegun Babaniyi and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 3 pooled it
8.9field-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

71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 129 citations in OpenAlex.

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11 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

15 authors at 7 institutions in 5 countries.

Perrine InquimbertCentre National de la Recherche Scientifique, UPR 3212, Institut des Neurosciences Cellulaires et Intégratives and Université de Strasbourg, 67084 Strasbourg, France; F.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Martin MollDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA; Institute of Pharmacology, Heidelberg University, 69120 Heidelberg, Germany.
Alban LatremoliereF.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA; Department of Neurology and Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Chi-Kun TongDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA.
John WhangDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA.
Gregory F SheehanDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA.
Brendan M SmithDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA.
Erica KorbLaboratory of Chromatin Biology and Epigenetics, Rockefeller University, New York, NY 10065, USA.
Maria C P AthiéDepartment of Structural and Functional Biology, State University of Campinas, Campinas, SP 13083-865, Brazil.
Olusegun BabaniyiF.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Nader GhasemlouF.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Yuchio YanagawaDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan.
C David AllisLaboratory of Chromatin Biology and Epigenetics, Rockefeller University, New York, NY 10065, USA.
Patrick R HofFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Joachim ScholzDepartments of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, NY 10032, USA. Electronic address: scholz.joachim@gmail.com.
Columbia University Irving Medical Center · USBoston Children's Hospital · USHarvard University · USRockefeller University · USAllen Institute for Brain Science · USGunma University · JPUniversidade Estadual de Campinas (UNICAMP) · BR

Funding

TRANSGENIC COREP01DA008227 · NIDA · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1993 to 2018
$28.1M
REPRESSIVE HISTONE AND DNA METHYLATION IN RODENT DEPRESSION MODELSP50MH096890 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI TAMMINGA, CAROL A · 2012 to 2021
$20.2M
Transsynaptic Neurodegeneration after Nerve InjuryR01NS050408 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI SCHOLZ, JOACHIM · 2007 to 2010
$1.2M
NIDA NIH HHS P01 DA008227NIMH NIH HHS P50 MH096890NINDS NIH HHS R01 NS050408
6 · The paper itself

Abstract

Peripheral nerve lesions provoke apoptosis in the dorsal horn of the spinal cord. The cause of cell death, the involvement of neurons, and the relevance for the processing of somatosensory information are controversial. Here, we demonstrate in a mouse model of sciatic nerve injury that glutamate-induced neurodegeneration and loss of γ-aminobutyric acid (GABA)ergic interneurons in the superficial dorsal horn promote the transition from acute to chronic neuropathic pain. Conditional deletion of Grin1, the essential subunit of N-methyl-d-aspartate-type glutamate receptors (NMDARs), protects dorsal horn neurons from excitotoxicity and preserves GABAergic inhibition. Mice deficient in functional NMDARs exhibit normal nociceptive responses and acute pain after nerve injury, but this initial increase in pain sensitivity is reversible. Eliminating NMDARs fully prevents persistent pain-like behavior. Reduced pain in mice lacking proapoptotic Bax confirmed the significance of neurodegeneration. We conclude that NMDAR-mediated neuron death contributes to the development of chronic neuropathic pain.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCell SurvivalChronic PainDown-Regulationgamma-Aminobutyric AcidGene DeletionGlutamatesMaleMice, Inbred C57BLNerve Tissue ProteinsNeuralgiaNeural InhibitionNeuroprotectionPeripheral Nerve Injuriesbcl-2-Associated X Proteingamma-Aminobutyric AcidGlutamatesGprin1 protein, mouseNerve Tissue ProteinsReceptors, N-Methyl-D-Aspartatechronic paindisinhibitiondorsal hornexcitotoxicitynerve injuryneuropathic painNMDA receptor

Identifiers

PMID29847798
PMCPMC6276118
OpenAlexW2807499669

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.