Evidence map›Paper›PMID 22131400›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Heterosynaptic long-term potentiation at GABAergic synapses of spinal lamina I neurons.

Henning Fenselau, Bernhard Heinke, Jürgen Sandkühler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  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. Inhibitory Plasticity: From Molecules to Computation and Beyond.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Heterosynaptic GABAergic plasticity bidirectionally driven by the activity of pre- and postsynaptic NMDA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Postsynaptic Depolarization Enhances GABA Drive to Dorsomedial Hypothalamic Neurons through Somatodendritic Cholecystokinin Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. Article
  16. Review
  17. GABA pharmacology: the search for analgesics.Neurochemical research · 2014
    Review
  18. Long-term potentiation of glycinergic synapses triggered by interleukin 1β.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  19. Article
  20. Remote optogenetic activation and sensitization of pain pathways in freely moving mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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

3 authors at 1 institution in 1 country.

Henning FenselauDepartment of Neurophysiology, Center for Brain Research, Medical University of Vienna, 1090 Vienna, Austria.
Bernhard Heinke
Jürgen Sandkühler
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons in spinal dorsal horn lamina I play a pivotal role for nociception that critically depends on a proper balance between excitatory and inhibitory inputs. Any modification in synaptic strength may challenge this delicate balance. Long-term potentiation (LTP) at glutamatergic synapses between nociceptive C-fibers and lamina I neurons is an intensively studied cellular model of pain amplification. In contrast, nothing is presently known about long-term changes of synaptic strength at inhibitory synapses in the spinal dorsal horn. Using a spinal cord-dorsal root slice preparation from rats, we show that conditioning stimulation of primary afferent fibers with a stimulating protocol that induces LTP at C-fiber synapses also triggered LTP at GABAergic synapses (LTP(GABA)). This LTP(GABA) was heterosynaptic in nature and was mediated by activation of group I metabotropic glutamate receptors. Opening of ionotropic glutamate receptor channels of the AMPA/KA or NMDA subtype was not required for LTP(GABA). Paired-pulse ratio, coefficient of variation, and miniature IPSCs analysis revealed that LTP(GABA) was expressed presynaptically. Nitric oxide as a retrograde messenger signal mediated this increase of GABA release at spinal inhibitory synapses. This novel form of synaptic plasticity in spinal nociceptive circuits may be an essential mechanism to maintain the relative balance between excitation and inhibition and to improve the signal-to-noise ratio in nociceptive pathways.

Indexed as

AnimalsElectric Stimulationgamma-Aminobutyric AcidInhibitory Postsynaptic PotentialsLong-Term PotentiationMaleNeurons, AfferentNitric OxideRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateSpinal CordSynapsesSynaptic Transmissiongamma-Aminobutyric AcidNitric OxideReceptors, Metabotropic Glutamate

Identifiers

PMID22131400
PMCPMC6623805
OpenAlexW1989685766

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.