Evidence map›Paper›PMID 19675290›Full record

ArticleJournal of neurophysiology2009

Activity-dependent modulation of glutamatergic signaling in the developing rat dorsal horn by early tissue injury.

Jie Li, Suellen M Walker, Maria Fitzgerald, Mark L Baccei

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Developmental mechanisms of CPSP: Clinical observations and translational laboratory evaluations.Canadian journal of pain = Revue canadienne de la douleur · 2022
    Review
  5. Article
  6. The development of pain circuits and unique effects of neonatal injury.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Long-Term Consequences of Neonatal Injury.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2015
    Review
  16. Cortex glial cells activation, associated with lowered mechanical thresholds and motor dysfunction, persists into adulthood after neonatal pain.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2014
    Article
  17. Review
  18. Review
  19. Review
  20. Neonatal pain.Paediatric anaesthesia · 2014
    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

4 authors.

Jie LiPain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, USA.
Suellen M Walker
Maria Fitzgerald
Mark L Baccei

Funding

Modulation of Developing Spinal Nociceptive Circuits by Sensory InputR03NS060858 · NINDS · UNIVERSITY OF CINCINNATI · PI BACCEI, MARK L · 2009 to 2010
$156k
Medical Research Council G0400572NINDS NIH HHS NS-060858NINDS NIH HHS R03 NS060858
6 · The paper itself

Abstract

Tissue injury in early life can produce distinctive effects on pain processing, but little is known about the underlying neural mechanisms. Neonatal inflammation modulates excitatory synapses in spinal nociceptive circuits, but it is unclear whether this results directly from altered afferent input. Here we investigate excitatory and inhibitory synaptic transmission in the rat superficial dorsal horn following neonatal hindlimb surgical incision using in vitro patch-clamp recordings and test the effect of blocking peripheral nerve activity on the injury-evoked changes. Surgical incision through the skin and muscle of the hindlimb at postnatal day 3 (P3) or P10 selectively increased the frequency, but not amplitude, of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) recorded 2-3 days after injury, without altering miniature inhibitory postsynaptic current frequency or amplitude at this time point. Meanwhile, incision at P17 failed to affect excitatory or inhibitory synaptic function at 2-3 days postinjury. The elevated mEPSC frequency was accompanied by increased inward rectification of evoked alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated currents, but no change in AMPAR/N-methyl-D-aspartate receptor ratios, and was followed by a persistent reduction in mEPSC frequency by 9-10 days postinjury. Prolonged blockade of primary afferent input from the time of injury was achieved by administration of bupivacaine hydroxide or tetrodotoxin to the sciatic nerve at P3. The increase in mEPSC frequency evoked by P3 incision was prevented by blocking sciatic nerve activity. These results demonstrate that increased afferent input associated with peripheral tissue injury selectively modulates excitatory synaptic drive onto developing spinal sensory neurons and that the enhanced glutamatergic signaling in the dorsal horn following neonatal surgical incision is activity dependent.

Indexed as

Anesthetics, LocalAnimalsAnimals, NewbornBupivacaineExcitatory Postsynaptic PotentialsGlutamic AcidIn Vitro TechniquesMuscle, SkeletalNerve BlockNeuronsPosterior Horn CellsRatsRats, Sprague-DawleyReceptors, AMPAReceptors, N-Methyl-D-AspartateSciatic NerveAnesthetics, LocalBupivacaineGlutamic AcidReceptors, AMPAReceptors, N-Methyl-D-AspartateTetrodotoxin

Identifiers

PMID19675290
PMCPMC2775379

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.