Evidence map›Paper›PMID 23639821›Full record

ArticlePain2013

Deficits in glycinergic inhibition within adult spinal nociceptive circuits after neonatal tissue damage.

Jie Li, Meredith L Blankenship, Mark L Baccei

Open access · greenAbstract read
In one paragraph

Article in Pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Early Life Injury Alters Spinal Astrocyte Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Neonatal Injury Evokes Persistent Deficits in Dynorphin Inhibitory Circuits within the Adult Mouse Superficial Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  7. Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020
    Review
  8. Neonatal Injury Alters Sensory Input and Synaptic Plasticity in GABAergic Interneurons of the Adult Mouse Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  9. Enhanced Postsynaptic GABANeuroscience · 2018
    Article
  10. Article
  11. Article
  12. Review
  13. Neonatal Tissue Damage Promotes Spike Timing-Dependent Synaptic Long-Term Potentiation in Adult Spinal Projection Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Long-Term Consequences of Neonatal Injury.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2015
    Review
  19. Aberrant synaptic integration in adult lamina I projection neurons following neonatal tissue damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Jie LiPain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA.
Meredith L Blankenship
Mark L Baccei
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

Developmental Regulation of Intrinsic Excitability in Spinal Pain NetworksR01NS072202 · NINDS · UNIVERSITY OF CINCINNATI · PI BACCEI, MARK L · 2010 to 2020
$3.4M
Modulation of Developing Spinal Nociceptive Circuits by Sensory InputR03NS060858 · NINDS · UNIVERSITY OF CINCINNATI · PI BACCEI, MARK L · 2009 to 2010
$156k
NINDS NIH HHS NS060858NINDS NIH HHS NS072202NINDS NIH HHS R01 NS072202NINDS NIH HHS R03 NS060858
6 · The paper itself

Abstract

Tissue injury during a critical period of early postnatal development can alter pain sensitivity throughout life. However, the degree to which neonatal tissue damage exerts prolonged effects on synaptic signaling within adult spinal nociceptive circuits remains unknown. Here we provide evidence that a transient surgical injury of the hind paw during the neonatal period compromises inhibitory transmission within the adult mouse superficial dorsal horn (SDH), while the same incision occurring during the third week of life failed to evoke these long-term modifications of the SDH synaptic network. The decrease in phasic inhibitory signaling after early tissue damage reflected a selective reduction in glycine receptor (GlyR)-mediated input onto both GABAergic and presumed glutamatergic neurons within lamina II of the adult SDH. Meanwhile, neonatal incision significantly decreased the density of tonic GlyR-mediated current only in the presumed glutamatergic population during adulthood. These persistent changes in synaptic function following early injury occurred in the absence of significant alterations in the transcription of genes known to be important for glycinergic transmission. These findings suggest that aberrant sensory input during early life has permanent consequences for the functional organization of nociceptive synaptic circuits within the adult spinal cord.

Indexed as

AgingNociceptionAnimalsAnimals, NewbornFemaleGlycineMiceMice, TransgenicNeural InhibitionPosterior Horn CellsReceptors, GlycineSoft Tissue InjuriesSpinal CordGlycineReceptors, Glycine

Identifiers

PMID23639821
PMCPMC3795070
OpenAlexW2085188038

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.