Evidence map›Paper›PMID 22287544›Full record

ArticleThe Journal of biological chemistry2012

Regulation of N-methyl-D-aspartic acid (NMDA) receptors by metabotropic glutamate receptor 7.

Zhenglin Gu, Wenhua Liu, Jing Wei, Zhen Yan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. PathogenicThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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.

Zhenglin GuDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York 14214.
Wenhua LiuDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York 14214.
Jing WeiDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York 14214.
Zhen YanDepartment of Physiology and Biophysics, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, New York 14214. Electronic address: zhenyan@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Functions of Dopamine D4 Receptors in Prefrontal CortexR01MH084233 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2008 to 2012
$1.8M
Synaptic Changes by Stress in Prefrontal CortexR01MH085774 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2010 to 2013
$1.2M
NIMH NIH HHS MH84233NIMH NIH HHS MH85774NIMH NIH HHS R01 MH084233NIMH NIH HHS R01 MH085774
6 · The paper itself

Abstract

Emerging evidence suggests that metabotropic glutamate receptors (mGluRs) are potential novel targets for brain disorders associated with the dysfunction of prefrontal cortex (PFC), a region critical for cognitive and emotional processes. Because N-methyl-D-aspartic acid receptor (NMDAR) dysregulation has been strongly associated with the pathophysiology of mental illnesses, we examined the possibility that mGluRs might be involved in modulating PFC functions by targeting postsynaptic NMDARs. We found that application of prototypical group III mGluR agonists significantly reduced NMDAR-mediated synaptic and ionic currents in PFC pyramidal neurons, which was mediated by mGluR7 localized at postsynaptic neurons and involved the β-arrestin/ERK signaling pathway. The mGluR7 modulation of NMDAR currents was prevented by agents perturbing actin dynamics and by the inhibitor of cofilin, a major actin-depolymerizing factor. Consistently, biochemical and immunocytochemical results demonstrated that mGluR7 activation increased cofilin activity and F-actin depolymerization via an ERK-dependent mechanism. Furthermore, mGluR7 reduced the association of NMDARs with the scaffolding protein PSD-95 and the surface level of NMDARs in an actin-dependent manner. These data suggest that mGluR7, by affecting the cofilin/actin signaling, regulates NMDAR trafficking and function. Because ablation of mGluR7 leads to a variety of behavioral symptoms related to PFC dysfunction, such as impaired working memory and reduced anxiety and depression, our results provide a potential mechanism for understanding the role of mGluR7 in mental health and disorders.

Indexed as

Synaptic TransmissionActin Depolymerizing FactorsActinsAnimalsAnxietyCells, CulturedDepressionDisks Large Homolog 4 ProteinGuanylate KinasesIntracellular Signaling Peptides and ProteinsMembrane ProteinsMemory DisordersMiceProtein TransportPyramidal CellsRatsActin Depolymerizing FactorsActinsDisks Large Homolog 4 ProteinDlg4 protein, mouseDlg4 protein, ratGuanylate KinasesIntracellular Signaling Peptides and ProteinsMembrane Proteinsmetabotropic glutamate receptor 7Receptors, Metabotropic GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22287544
PMCPMC3322988
OpenAlexW2114397675

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.