Evidence map›Paper›PMID 22761940›Full record

ArticlePloS one2012

Current and calcium responses to local activation of axonal NMDA receptors in developing cerebellar molecular layer interneurons.

Bénédicte Rossi, David Ogden, Isabel Llano, Yusuf P Tan, Alain Marty, Thibault Collin

Abstract read
In one paragraph

Article in PloS one, 2012. 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
–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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Recurrent Circuits Amplify Corticofugal Signals and Drive Feedforward Inhibition in the Inferior Colliculus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Influence of spatially segregated IPProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Temporal integration and 1/Journal of neurophysiology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors.

Bénédicte RossiLaboratoire de Physiologie Cérébrale, CNRS-UMR 8118, Université Paris Descartes, Université Paris Diderot, Paris, France.
David Ogden
Isabel Llano
Yusuf P Tan
Alain Marty
Thibault Collin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In developing cerebellar molecular layer interneurons (MLIs), NMDA increases spontaneous GABA release. This effect had been attributed to either direct activation of presynaptic NMDA receptors (preNMDARs) or an indirect pathway involving activation of somato-dendritic NMDARs followed by passive spread of somatic depolarization along the axon and activation of axonal voltage dependent Ca(2+) channels (VDCCs). Using Ca(2+) imaging and electrophysiology, we searched for preNMDARs by uncaging NMDAR agonists either broadly throughout the whole field or locally at specific axonal locations. Releasing either NMDA or glutamate in the presence of NBQX using short laser pulses elicited current transients that were highly sensitive to the location of the spot and restricted to a small number of varicosities. The signal was abolished in the presence of high Mg(2+) or by the addition of APV. Similar paradigms yielded restricted Ca(2+) transients in interneurons loaded with a Ca(2+) indicator. We found that the synaptic effects of NMDA were not inhibited by blocking VDCCs but were impaired in the presence of the ryanodine receptor antagonist dantrolene. Furthermore, in voltage clamped cells, bath applied NMDA triggers Ca(2+) elevations and induces neurotransmitter release in the axonal compartment. Our results suggest the existence of preNMDARs in developing MLIs and propose their involvement in the NMDA-evoked increase in GABA release by triggering a Ca(2+)-induced Ca(2+) release process mediated by presynaptic Ca(2+) stores. Such a mechanism is likely to exert a crucial role in various forms of Ca(2+)-mediated synaptic plasticity.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingCerebellumInterneuronsRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateCalciumCalcium ChannelsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22761940
PMCPMC3384623

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Registered trials

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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.