Evidence map›Paper›PMID 23707311›Full record

ArticlePain2013

Non-Hebbian plasticity at C-fiber synapses in rat spinal cord lamina I neurons.

Asami Naka, Doris Gruber-Schoffnegger, Jürgen Sandkühler

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. 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
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. TARP γ-2 Is Required for Inflammation-Associated AMPA Receptor Plasticity within Lamina II of the Spinal Cord Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  17. Article
  18. Periaqueductal Grey EP3 Receptors Facilitate Spinal Nociception in Arthritic Secondary Hypersensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  19. Article
  20. Selective activation of microglia facilitates synaptic strength.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Asami NakaDepartment of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.
Doris Gruber-Schoffnegger
Jürgen Sandkühler
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current concepts of memory storage are largely based on Hebbian-type synaptic long-term potentiation induced by concurrent activity of pre- and postsynaptic neurons. Little is known about non-Hebbian synaptic plasticity, which, if present in nociceptive pathways, could resolve a number of unexplained findings. We performed whole-cell patch-clamp recordings in rat spinal cord slices and found that a rise in postsynaptic [Ca(2+)]i due to postsynaptic depolarization was sufficient to induce synaptic long-term potentiation (LTP) in the absence of any presynaptic conditioning stimulation. LTP induction could be prevented by postsynaptic application of the Ca(2+) chelator BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid), the L-type voltage-gated calcium channel (VGCC) antagonist nifedipine, and by postsynaptic application of the NMDA receptor antagonist MK801. This indicates that synaptic potentiation was induced postsynaptically by Ca(2+) entry likely via L-type voltage-gated Ca(2+) channels (VGCC) and via NMDA receptor channels. The paired pulse ratio and the coefficient of variation remained unchanged in neurons expressing LTP, suggesting that this form of synaptic potentiation was not only induced, but also expressed postsynaptically. Postsynaptic depolarization had no influence on firing patterns, action potential shape, or neuronal excitability. An increase in [Ca(2+)]i in spinal lamina I neurons induces a non-Hebbian form of synaptic plasticity in spinal nociceptive pathways without affecting neuronal active and passive membrane properties.

Indexed as

AnimalsAnimals, NewbornCalciumCalcium Channel BlockersDizocilpine MaleateElectric StimulationExcitatory Amino Acid AntagonistsIn Vitro TechniquesLong-Term PotentiationMaleNerve Fibers, UnmyelinatedNeuronsNifedipinePatch-Clamp TechniquesRatsRats, Sprague-DawleyCalciumCalcium Channel BlockersDizocilpine MaleateExcitatory Amino Acid AntagonistsNifedipineRyanodine

Identifiers

PMID23707311
PMCPMC3708128
OpenAlexW2052275590

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.