Evidence map›Paper›PMID 19926678›Full record

ReviewPharmacological reviews2009

Metabotropic glutamate receptor-mediated long-term depression: molecular mechanisms.

Clare M Gladding, Stephen M Fitzjohn, Elek Molnár

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

121 citing papers in PubMed, 227 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Spontaneous glutamate release activates mGluR signaling to drive rapid antidepressant responses.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Quantification of [Current neuropharmacology · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Enhanced mGluRCell death & disease · 2024
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

61 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

3 authors at 1 institution in 1 country.

Clare M GladdingMRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, School of Medical Sciences, University Walk, Bristol, BS8 1TD, UK.
Stephen M Fitzjohn
Elek Molnár
University of Bristol · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F011326/1Medical Research Council 57294Medical Research Council 80049Medical Research Council G0601509
6 · The paper itself

Abstract

The ability to modify synaptic transmission between neurons is a fundamental process of the nervous system that is involved in development, learning, and disease. Thus, synaptic plasticity is the ability to bidirectionally modify transmission, where long-term potentiation and long-term depression (LTD) represent the best characterized forms of plasticity. In the hippocampus, two main forms of LTD coexist that are mediated by activation of either N-methyl-d-aspartic acid receptors (NMDARs) or metabotropic glutamate receptors (mGluRs). Compared with NMDAR-LTD, mGluR-LTD is less well understood, but recent advances have started to delineate the underlying mechanisms. mGluR-LTD at CA3:CA1 synapses in the hippocampus can be induced either by synaptic stimulation or by bath application of the group I selective agonist (R,S)-3,5-dihydroxyphenylglycine. Multiple signaling mechanisms have been implicated in mGluR-LTD, illustrating the complexity of this form of plasticity. This review provides an overview of recent studies investigating the molecular mechanisms underlying hippocampal mGluR-LTD. It highlights the role of key molecular components and signaling pathways that are involved in the induction and expression of mGluR-LTD and considers how the different signaling pathways may work together to elicit a persistent reduction in synaptic transmission.

Indexed as

AnimalsExcitatory Amino Acid AgonistsHumansLong-Term Synaptic DepressionNeuronsReceptors, Metabotropic GlutamateExcitatory Amino Acid AgonistsReceptors, Metabotropic Glutamate

Identifiers

PMID19926678
PMCPMC2802426
OpenAlexW2169371082

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.