Evidence map›Paper›PMID 22626985›Full record

ReviewNeuropharmacology2013

Role of presynaptic metabotropic glutamate receptors in the induction of long-term synaptic plasticity of vesicular release.

Chirag Upreti, Xiao-Lei Zhang, Simon Alford, Patric K Stanton

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Metabotropic Glutamate Receptors Modulate Exocytotic Tau Release and Propagation.The Journal of pharmacology and experimental therapeutics · 2022
    Article
  4. Article
  5. Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments.International journal of molecular sciences · 2021
    Review
  6. Review
  7. The auxiliary glutamate receptor subunit dSol-1 promotes presynaptic neurotransmitter release and homeostatic potentiation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Synaptic plasticity mechanisms common to learning and alcohol use disorder.Learning & memory (Cold Spring Harbor, N.Y.) · 2018
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Chirag UpretiDepartment of Cell Biology & Anatomy, New York Medical College, Valhalla, NY 10595, USA.
Xiao-Lei Zhang
Simon Alford
Patric K Stanton
New York Medical College · USUniversity of Illinois Chicago · US

Funding

Presynaptic Mechanisms of Long-Term DepressionR01NS044421 · NINDS · YESHIVA UNIVERSITY · PI STANTON, PATRIC K. · 2003 to 2012
$3.0M
Synaptic Plasticity and the Dynamic Interactions Between Calcium and PresynapticR01MH084874 · NIMH · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALFORD, SIMON T · 2010 to 2014
$1.9M
PRESYNAPTIC LONG-TERM SYNAPTIC DEPRESSIONR56NS044421 · NINDS · NEW YORK MEDICAL COLLEGE · PI STANTON, PATRIC K. · 2008 to 2008
$413k
NIMH NIH HHS R01 MH084874NINDS NIH HHS R01 NS044421NINDS NIH HHS R56 NS044421
6 · The paper itself

Abstract

While postsynaptic ionotropic and metabotropic glutamate receptors have received the lions share of attention in studies of long-term activity-dependent synaptic plasticity, it is becoming clear that presynaptic metabotropic glutamate receptors play critical roles in both short-term and long-term plasticity of vesicular transmitter release, and that they act both at the level of voltage-dependent calcium channels and directly on proteins of the vesicular release machinery. Activation of G protein-coupled receptors can transiently inhibit vesicular release through the release of Gβγ which binds to both voltage-dependent calcium channels to reduce calcium influx, and directly to the C-terminus region of the SNARE protein SNAP-25. Our recent work has revealed that the binding of Gβγ to SNAP-25 is necessary, but not sufficient, to elicit long-term depression (LTD) of vesicular glutamate release, and that the concomitant release of Gα(i) and the second messenger nitric oxide are also necessary steps in the presynaptic LTD cascade. Here, we review the current state of knowledge of the molecular steps mediating short-term and long-term plasticity of vesicular release at glutamatergic synapses, and the many gaps that remain to be addressed. This article is part of a Special Issue entitled 'Metabotropic Glutamate Receptors'.

Indexed as

AnimalsBrainCalcium ChannelsNeural Networks, ComputerNeuronal PlasticityPresynaptic TerminalsReceptors, G-Protein-CoupledReceptors, Metabotropic GlutamateSynaptic TransmissionSynaptic VesiclesSynaptosomal-Associated Protein 25Calcium ChannelsReceptors, G-Protein-CoupledReceptors, Metabotropic GlutamateSynaptosomal-Associated Protein 25

Identifiers

PMID22626985
PMCPMC3432151
OpenAlexW1966803934

What OpenQuestion holds

Textmetadata
LicenceTDM
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.