Evidence map›Paper›PMID 11711567›Full record

ArticleThe Journal of physiology2001

Retrograde modulation of transmitter release by postsynaptic subtype 1 metabotropic glutamate receptors in the rat cerebellum.

C Levenes, H Daniel, F Crepel

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Astrocytes display complex and localized calcium responses to single-neuron stimulation in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  5. Article
  6. Somatodendritic release of glutamate regulates synaptic inhibition in cerebellar Purkinje cells via autocrine mGluR1 activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  7. NMDA receptor contribution to the climbing fiber response in the adult mouse Purkinje cell.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  8. Properties of persistent postnatal cortical subplate neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  9. Article
  10. Maintenance of presynaptic function by AMPA receptor-mediated excitatory postsynaptic activity in adult brain.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  11. Article
  12. Article
  13. Group I metabotropic glutamate receptors inhibit GABA release at interneuron-Purkinje cell synapses through endocannabinoid production.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  14. Review
  15. Article
  16. Article
  17. 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.

C LevenesLaboratoire de Neurobiologie et Neuropharmacologie du Développement, Institut des Neurosciences, CNRS, UMR C7624, 7, quai St Bernard, 75005 Paris, France. carole.levenes@snv.jussieu.fr
H Daniel
F Crepel
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The aim of the study was to elucidate the mechanisms underlying the depressant effect of the group I/II metabotropic glutamate receptor (mGluR) agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) on parallel fibre (PF) to Purkinje cell (PC) synaptic transmission. Experiments were performed in rat cerebellar slices using the whole-cell patch-clamp technique and fluorometric measurements of presynaptic calcium variation 2. Analysis of short-term plasticity, fluctuation of EPSC amplitude and responses of PCs to exogenous glutamate showed that depression caused by 1S,3R-ACPD is presynaptic. 3. The effects of 1S,3R-ACPD were blocked and reproduced by group I mGluR antagonists and agonists, respectively. 4. These effects remained unchanged in mGluR5 knock-out mice and disappeared in mGluR1 knock-out mice. 5. 1S,3R-ACPD increased calcium concentration in PFs. This effect was abolished by AMPA/kainate (but not NMDA) receptor antagonists and mimicked by focally applied agonists of these receptors. Thus, it is not directly due to mGluRs but to presynaptic AMPA/kainate receptors indirectly activated by 1S,3R-ACPD. 6. Frequencies of spontaneous and evoked unitary EPSCs recorded in PCs were respectively increased and decreased by mGluR1 agonists. Similar results were obtained when mGluR1s were activated by tetanic stimulation of PFs. 7. Injecting 30 mM BAPTA into PCs blocked the effects of 1S,3R-ACPD on unitary EPSCs. 8. In conclusion, 1S,3R-ACPD reduces evoked release of glutamate from PFs. This effect is triggered by postsynaptic mGluR1s and thus implies that a retrograde messenger, probably glutamate, opens presynaptic AMPA/kainate receptors and consequently increases spontaneous release of glutamate from PF terminals and decreases evoked synaptic transmission.

Indexed as

AnimalsCerebellumCycloleucineExcitatory Postsynaptic PotentialsGlutamic AcidIn Vitro TechniquesMaleMiceMice, KnockoutNerve FibersNeurotransmitter AgentsPresynaptic TerminalsRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateSynapses1-amino-1,3-dicarboxycyclopentaneCycloleucineGlutamic Acidmetabotropic glutamate receptor type 1Neurotransmitter AgentsReceptors, Metabotropic Glutamate

Identifiers

PMID11711567
PMCPMC2278923
OpenAlexW2153327525

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.