Evidence map›Paper›PMID 10393888›Full record

ReviewProceedings of the National Academy of Sciences of the United States of America1999

Transcriptional and posttranslational plasticity and the generation of inflammatory pain.

C J Woolf, M Costigan

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 2 pooled it
11.3field-weighted citation impact, top 1% 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

155 citing papers in PubMed, 2 syntheses or guidelines pooled it, 551 citations in OpenAlex.

  1. Pooled it
  2. Antidepressants for pain management in rheumatoid arthritis.The Cochrane database of systematic reviews · 2011
    Pooled it
  3. Trial
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  15. The role of neurotrophic factors in novel, rapid psychiatric treatments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Review
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  17. Review
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  19. Effects ofJournal of advanced veterinary and animal research · 2022
    Article
  20. Review

95 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.

C J WoolfNeural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Massachusetts General Hospital-East, Charlestown, MA 02129, USA. woolf.clifford@mgh.harvard.edu
M Costigan
Massachusetts General Hospital · US

Funding

ALTERED SENSIBILITY FOLLOWING PERIPHERAL NERVE DAMAGER01NS038253 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI WOOLF, CLIFFORD J · 1999 to 2017
$8.2M
NINDS NIH HHS R01 NS038253NINDS NIH HHS R01 NS38253-01Wellcome Trust
6 · The paper itself

Abstract

Inflammatory pain manifests as spontaneous pain and pain hypersensitivity. Spontaneous pain reflects direct activation of specific receptors on nociceptor terminals by inflammatory mediators. Pain hypersensitivity is the consequence of early posttranslational changes, both in the peripheral terminals of the nociceptor and in dorsal horn neurons, as well as later transcription-dependent changes in effector genes, again in primary sensory and dorsal horn neurons. This inflammatory neuroplasticity is the consequence of a combination of activity-dependent changes in the neurons and specific signal molecules initiating particular signal-transduction pathways. These pathways phosphorylate membrane proteins, changing their function, and activate transcription factors, altering gene expression. Two distinct aspects of sensory neuron function are changed as a result of these processes, basal sensitivity, or the capacity of peripheral stimuli to evoke pain, and stimulus-evoked hypersensitivity, the capacity of certain inputs to generate prolonged alterations in the sensitivity of the system. Posttranslational changes largely alter basal sensitivity. Transcriptional changes both potentiate the system and alter neuronal phenotype. Potentiation occurs as a result of the up-regulation in the dorsal root ganglion of centrally acting neuromodulators and simultaneously in the dorsal horn of their receptors. This means that the response to subsequent inputs is augmented, particularly those that induce stimulus-induced hypersensitivity. Alterations in phenotype includes the acquisition by A fibers of neurochemical features typical of C fibers, enabling these fibers to induce stimulus-evoked hypersensitivity, something only C fiber inputs normally can do. Elucidation of the molecular mechanisms responsible provides new opportunities for therapeutic approaches to managing inflammatory pain.

Indexed as

Protein Processing, Post-TranslationalTranscription, GeneticAnimalsGanglia, SpinalHumansInflammationNeurons, AfferentNociceptorsPainReceptors, Cell SurfaceSomatosensory CortexSpinal CordReceptors, Cell Surface

Identifiers

PMID10393888
PMCPMC33609
OpenAlexW2040035374

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.