Evidence map›Paper›PMID 1359126›Full record

ArticleThe Journal of physiology1992

Activation and desensitization of N-methyl-D-aspartate receptors in nucleated outside-out patches from mouse neurones.

W Sather, S Dieudonné, J F MacDonald, P Ascher

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
4.5field-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

113 citing papers in PubMed, 237 citations in OpenAlex.

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  12. Distinct roles ofF1000Research · 2019
    Review
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. NMDA Receptors in the Central Nervous System.Methods in molecular biology (Clifton, N.J.) · 2017
    Article
  20. Article

53 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 1 institution in 1 country.

W SatherLaboratoire de Neurobiologie, Ecole Normale Supérieure, Paris, France.
S Dieudonné
J F MacDonald
P Ascher
Laboratoire de Géologie de l’École Normale Supérieure · FR

Funding

QUISQUALATE-ACTIVATED CONDUCTANCE CHANGE MEDIATED BY IP3F32NS008562 · NINDS · ECOLE NORMALE SUPERIEURE · PI SATHER, WILLIAM A · 1988 to 1990
–
NINDS NIH HHS 1 F 32 NS08562
6 · The paper itself

Abstract

1. Activation and desensitization of N-methyl-D-aspartate (NMDA) receptors were studied in large outside-out patches excised from cultured embryonic neurones dissociated from mouse forebrain. The patches were exposed to rapid changes of NMDA or L-glutamate concentrations in the presence of glycine at concentrations (10-20 microM) saturating the modulatory site of the NMDA receptor. 2. Immediately after formation of the patch the responses to NMDA and L-glutamate showed a slow and small desensitization, even with high concentrations of agonist. During the following hour, the peak response either decreased or remained relatively stable, but in all cases the desensitization increased and accelerated until it stabilized. In this 'stabilized' state, the desensitization produced by high concentrations of NMDA (1 mM) or L-glutamate (300 microM) had an exponential time course, with a time constant of about 30 ms. The ratio of the peak over the steady-state current was in the order of 40 for NMDA and about 30 for L-glutamate. 3. Concentration-response curves were built for the peak and the plateau responses, for NMDA and for L-glutamate. The comparison of these curves indicated that (i) the EC50 of the peak (K(app) was always higher than the EC50 of the plateau (Kss); (ii) the two EC50 values for NMDA (K(app) and Kss) were higher than those for L-glutamate; (iii) the Hill coefficient was close to 1.4 for each of the four curves. 4. The application of NMDA or L-glutamate at a low concentration for 3 s periods reduced the response to a subsequent application of the same agonist at a saturating concentration. The IC50 of this 'predesensitization', termed Kpre, was lower than the EC50 of the steady-state response, Kss. 5. The onset rates of desensitization increased with the concentration of agonist. The EC50 of this relation was close to the value of K(app). 6. The decay of the currents at the end of a 3 s application of agonist was usually well described by the sum of two exponentials both of which were faster for NMDA than for L-glutamate. 7. The recovery from desensitization after a long (3 s) pulse of agonist was approximately exponential, with a time constant of about 0.5 s for NMDA and about 3.5 s for L-glutamate.(ABSTRACT TRUNCATED AT 400 WORDS)

Indexed as

AnimalsCells, CulturedElectrophysiologyGlutamatesGlutamic AcidKineticsMiceModels, ChemicalNeuronsN-MethylaspartateReceptors, N-Methyl-D-AspartateGlutamatesGlutamic AcidN-MethylaspartateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID1359126
PMCPMC1176143
OpenAlexW2003184890

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.