Evidence map›Paper›PMID 9204921›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

A long-lasting calcium-activated nonselective cationic current is generated by synaptic stimulation or exogenous activation of group I metabotropic glutamate receptors in CA1 pyramidal neurons.

P Congar, X Leinekugel, Y Ben-Ari, V Crépel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Alteration in CaMolecular biology reports · 2025
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  10. CaEpilepsia · 2017
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  11. Article
  12. Neurological and Motor Disorders: Neuronal Store-Operated CaAdvances in experimental medicine and biology · 2017
    Review
  13. Differential Contribution of CaFrontiers in cellular neuroscience · 2017
    Article
  14. PERK regulates GMolecular brain · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Group I mGluRs evoke K-ATP current by intracellular Ca2+ mobilization in rat subthalamus neurons.The Journal of pharmacology and experimental therapeutics · 2013
    Article
  19. Metabotropic glutamate receptors drive global persistent inhibition in the visual thalamus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  20. The cellular building blocks of breathing.Comprehensive Physiology · 2012
    Review

3 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

P CongarUniversité René Descartes and Institut National de la Santé et de la Recherche Médicale Unité 29, 75674 Paris Cedex 14, France.
X Leinekugel
Y Ben-Ari
V Crépel
Université Paris Cité · FRDélégation Paris 5 · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have shown previously that a selective metabotropic glutamate receptor (mGluR) agonist, 1S,3R-1-aminocyclo-pentane-1, 3-dicarboxylate (1S,3R-ACPD), evokes an inward current in CA1 pyramidal neurons of rat hippocampal slices in the presence of K+ channel blockers (). This current has been characterized as a Ca2+-activated nonselective cationic (CAN) current. Using whole-cell patch-clamp recordings and intracellular dialysis, we now have identified the mGluR subtype and the mechanisms underlying the CAN current (ICAN) and report for the first time the presence of a synaptic ICAN in the mammalian CNS. First, we have shown pharmacologically that activation of ICAN by 1S,3R-ACPD involves the group I mGluRs (and not the groups II and III) and a G-protein-dependent process. We also report that ICAN is modulated by the divalent cations (Mg2+, Cd2+, and Zn2+). Second, we have isolated a slow synaptic inward current evoked by a high-frequency stimulation in the presence of K+ channel blockers, ionotropic glutamate, and GABAA receptor antagonists. This current shows similar properties to the exogenously evoked ICAN: its reversal potential is close to the reversal potential of the 1S, 3R-ACPD-evoked ICAN, and it is G-protein- and Ca2+-dependent. Because the amplitude and duration of ICAN increased in the presence of a glutamate uptake blocker, we suggest that this synaptic current is generated via the activation of mGluRs. We propose that the synaptic ICAN, activated by a brief tetanic stimulation and leading to a long-lasting inward current, may be involved in neuronal plasticity and synchronized network-driven oscillations.

Indexed as

AnimalsCalciumCationsCycloleucineIon TransportMaleNeuroprotective AgentsPatch-Clamp TechniquesPyramidal CellsRatsRats, WistarReceptors, Metabotropic GlutamateSynaptic TransmissionTime Factors1-amino-1,3-dicarboxycyclopentaneCalciumCationsCycloleucineNeuroprotective AgentsReceptors, Metabotropic Glutamate

Identifiers

PMID9204921
PMCPMC6793810
OpenAlexW2170571477

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.