Evidence map›Paper›PMID 12972628›Full record

ArticleThe Journal of physiology2003

Kinetic properties of the alpha2 homo-oligomeric glycine receptor impairs a proper synaptic functioning.

J M Mangin, M Baloul, L Prado De Carvalho, B Rogister, J M Rigo, P Legendre

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

41 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Human GlyRα2 pore dynamics in gating and inhibition.Structure (London, England : 1993) · 2026
    Article
  3. Review
  4. Role of the Glycine Receptor β Subunit in Synaptic Localization and Pathogenicity in Severe Startle Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. The GLRA1 missense mutation W170S associates lack of Zn2+ potentiation with human hyperekplexia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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 at 3 institutions in 2 countries.

J M ManginUMR CNRS 7102 Neurobiologie des Processus Adaptatifs, Université Pierre et Marie Curie, 9 quai St Bernard, 75252 Paris cedex 05, France. jmmangin@snv.jussieu.fr
M Baloul
L Prado De Carvalho
B Rogister
J M Rigo
P Legendre
Sorbonne Université · FRUniversity of Liège · BECentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionotropic glycine receptors (GlyRs) are present in the central nervous system well before the establishment of synaptic contacts. Immature nerve cells are known, at least in the spinal cord, to express alpha2 homomeric GlyRs, the properties of which are relatively unknown compared to those of the adult synaptic form of the GlyR (mainly alpha1/beta heteromeres). Here, the kinetics properties of GlyRs at the single-channel level have been recorded in real-time by means of the patch-clamp technique in the outside-out configuration coupled with an ultra-fast flow application system (< 100 micros). Recordings were performed on chinese hamster ovary (CHO) cells stably transfected with the alpha2 GlyR subunit. We show that the onset, the relaxation and the desensitisation of alpha2 homomeric GlyR-mediated currents are slower by one or two orders of magnitude compared to synaptic mature GlyRs and to other ligand-gated ionotropic channels involved in fast synaptic transmission. First latency analysis performed on single GlyR channels revealed that their slow activation time course was due to delayed openings. When synaptic release of glycine was mimicked (1 mM glycine; 1 ms pulse duration), the opening probability of alpha2 homomeric GlyRs was low (P(o) approximately = 0.1) when compared to mature synaptic GlyRs (Po = 0.9). This low Po is likely to be a direct consequence of the relatively slow activation kinetics of alpha2 homomeric GlyRs when compared to the activation kinetics of mature alpha1/beta GlyRs. Such slow kinetics suggest that embryonic alpha2 homomeric GlyRs cannot be activated by fast neurotransmitter release at mature synapses but rather could be suited for a non-synaptic paracrine-like release of agonist, which is known to occur in the embryo.

Indexed as

AlgorithmsAnimalsCHO CellsComputer SimulationCricetinaeCricetulusDimerizationDose-Response Relationship, DrugElectronic Data ProcessingGlycineKineticsMembrane PotentialsModels, BiologicalParacrine CommunicationPatch-Clamp TechniquesReceptors, GlycineGlycineReceptors, Glycine

Identifiers

PMID12972628
PMCPMC2343566
OpenAlexW2131925023

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.