Evidence map›Paper›PMID 27170136›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Neonatal Tissue Damage Promotes Spike Timing-Dependent Synaptic Long-Term Potentiation in Adult Spinal Projection Neurons.

Jie Li, Mark L Baccei

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Early Life Injury Alters Spinal Astrocyte Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  4. Article
  5. Article
  6. Cell Type-Dependent Short-Term Plasticity and Dopaminergic Modulation of Sensory Synapses onto Mouse Superficial Dorsal Horn Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  7. Article
  8. Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Early Life Pain Experience Changes Adult Functional Pain Connectivity in the Rat Somatosensory and the Medial Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  13. Article
  14. Review
  15. Intracellular Calcium Responses Encode Action Potential Firing in Spinal Cord Lamina I Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. 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
  17. The development of pain circuits and unique effects of neonatal injury.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  18. Article
  19. 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
  20. Article
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.

Jie LiPain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267.
Mark L BacceiPain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267 mark.baccei@uc.edu.
University of Cincinnati Medical Center · US

Funding

Synaptic Function within Mature Central Pain Networks after Neonatal InjuryR01NS080889 · NINDS · UNIVERSITY OF CINCINNATI · PI Mark L Baccei · 2013 to 2026
$4.5M
NINDS NIH HHS R01 NS080889
6 · The paper itself

Abstract

unlabelledMounting evidence from both humans and rodents suggests that tissue damage during the neonatal period can "prime" developing nociceptive pathways such that a subsequent injury during adulthood causes an exacerbated degree of pain hypersensitivity. However, the cellular and molecular mechanisms that underlie this priming effect remain poorly understood. Here, we demonstrate that neonatal surgical injury relaxes the timing rules governing long-term potentiation (LTP) at mouse primary afferent synapses onto mature lamina I projection neurons, which serve as a major output of the spinal nociceptive network and are essential for pain perception. In addition, whereas LTP in naive mice was only observed if the presynaptic input preceded postsynaptic firing, early tissue injury removed this temporal requirement and LTP was observed regardless of the order in which the inputs were activated. Neonatal tissue damage also reduced the dependence of spike-timing-dependent LTP on NMDAR activation and unmasked a novel contribution of Ca(2+)-permeable AMPARs. These results suggest for the first time that transient tissue damage during early life creates a more permissive environment for the production of LTP within adult spinal nociceptive circuits. This persistent metaplasticity may promote the excessive amplification of ascending nociceptive transmission to the mature brain and thereby facilitate the generation of chronic pain after injury, thus representing a novel potential mechanism by which early trauma can prime adult pain pathways in the CNS. SIGNIFICANCE STATEMENT: Tissue damage during early life can "prime" developing nociceptive pathways in the CNS, leading to greater pain severity after repeat injury via mechanisms that remain poorly understood. Here, we demonstrate that neonatal surgical injury widens the timing window during which correlated presynaptic and postsynaptic activity can evoke long-term potentiation (LTP) at sensory synapses onto adult lamina I projection neurons, which serve as a major output of the spinal nociceptive circuit and are essential for pain perception. This persistent increase in the likelihood of LTP induction after neonatal injury is predicted to favor the excessive amplification of ascending nociceptive transmission to the mature brain in response to subsequent injury and thereby exacerbate chronic pain.

Indexed as

Long-Term PotentiationNociceptionAfferent PathwaysAnimalsCalciumFemaleMiceNeurons, AfferentPain PerceptionReceptors, AMPAReceptors, N-Methyl-D-AspartateSoft Tissue InjuriesSpinal CordCalciumReceptors, AMPAReceptors, N-Methyl-D-Aspartatedevelopmentdorsal horninjuryspinal cordsynaptic plasticity

Identifiers

PMID27170136
PMCPMC4863065
OpenAlexW2390672039

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.