Evidence map›Paper›PMID 21129167›Full record

ReviewCNS neuroscience & therapeutics2011

Therapeutic potential of kainate receptors.

Carlos Matute

Open access · bronzeAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Structure and gating of kainate receptors.Frontiers in pharmacology · 2025
    Review
  6. Article
  7. Article
  8. Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

1 author at 1 institution in 1 country.

Carlos MatuteCentro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas (CIBERNED) and Departamento de Neurociencias, Universidad del País Vasco, 48940-Leioa, Spain. carlos.matute@ehu.es
University of the Basque Country · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamate receptors are key mediators of brain communication. Among ionotropic glutamate receptors, kainate receptors (KARs) have been least explored and their relevance to pathophysiology is relatively obscure. This is in part due to the relatively low abundance of KARs, the regulatory function in network activity they play, the lack of specific agonists and antagonists for this receptor subtype, as well as to the absence of striking phenotypes in mice deficient in KAR subunits. Nonetheless, it is now well established that KARs are located presynaptically whereby they regulate glutamate and GABA release, and thus, excitability and participate in short-term plasticity. In turn, KARs are also located postsynaptically and their activation contributes to synaptic integration. The development of specific novel ligands is helping to further investigate the contribution of KARs to health and disease. In this review, I summarize current knowledge about KAR physiology and pharmacology, and discuss their involvement in cell death and disease. In addition, I recapitulate the available data about the use of KAR antagonists and receptor subunit deficient mice in experimental paradigms of brain diseases, as well as the main findings about KAR roles in human CNS disorders. In sum, subunit specific antagonists have therapeutic potential in neurodegenerative and psychiatric diseases as well as in epilepsy and pain. Knowledge about the genetics of KARs will also help to understand the pathophysiology of those and other illnesses.

Indexed as

AnalgesicsAnimalsAnimals, Genetically ModifiedAnticonvulsantsCell DeathCentral Nervous System AgentsEpilepsyHumansKainic Acid ReceptorsMental DisordersMiceMice, KnockoutNeurodegenerative DiseasesPainStrokeAnalgesicsAnticonvulsantsCentral Nervous System AgentsKainic Acid Receptors

Identifiers

PMID21129167
PMCPMC3430855
OpenAlexW1516847526

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.