Evidence map›Paper›PMID 11312279›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Kainate receptors depress excitatory synaptic transmission at CA3-->CA1 synapses in the hippocampus via a direct presynaptic action.

M Frerking, D Schmitz, Q Zhou, J Johansen, R A Nicoll

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.3field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Article
  6. Review
  7. Influence of glutamate and GABA transport on brain excitatory/inhibitory balance.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Kainate Receptors Inhibit Glutamate Release Via Mobilization of Endocannabinoids in Striatal Direct Pathway Spiny Projection Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Glutamate receptors, neurotoxicity and neurodegeneration.Pflugers Archiv : European journal of physiology · 2010
    Review
  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

5 authors at 1 institution in 1 country.

M FrerkingDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, California 94143-0450, USA.
D Schmitz
Q Zhou
J Johansen
R A Nicoll
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kainate receptor activation depresses synaptic release of neurotransmitter at a number of synapses in the CNS. The mechanism underlying this depression is controversial, and both ionotropic and metabotropic mechanisms have been suggested. We report here that the AMPA/kainate receptor agonists domoate (DA) and kainate (KA) cause a presynaptic depression of glutamatergic transmission at CA3-->CA1 synapses in the hippocampus, which is not blocked by the AMPA receptor antagonist GYKI 53655 but is blocked by the AMPA/KA receptor antagonist CNQX. Neither a blockade of interneuronal discharge nor antagonists of several neuromodulators affect the depression, suggesting that it is not the result of indirect excitation and subsequent release of a neuromodulator. Presynaptic depolarization, achieved via increasing extracellular K(+), caused a depression of the presynaptic fiber volley and an increase in the frequency of miniature EPSCs. Neither effect was observed with DA, suggesting that DA does not depress transmission via a presynaptic depolarization. However, the effects of DA were abolished by the G-protein inhibitors N-ethylmaleimide and pertussis toxin. These results suggest that KA receptor activation depresses synaptic transmission at this synapse via a direct, presynaptic, metabotropic action.

Indexed as

AnimalsDose-Response Relationship, DrugEnzyme InhibitorsEthylmaleimideExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGTP-Binding ProteinsHippocampusIn Vitro TechniquesKainic AcidKainic Acid ReceptorsPatch-Clamp TechniquesPertussis ToxinPotassiumRatsdomoic acidEnzyme InhibitorsEthylmaleimideExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsGTP-Binding ProteinsKainic AcidKainic Acid ReceptorsPertussis ToxinPotassiumReceptors, AMPAVirulence Factors, Bordetella

Identifiers

PMID11312279
PMCPMC6762553
OpenAlexW2143563675

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.