Evidence map›Paper›PMID 27543109›Full record

ArticleMolecular brain2016

Orchestrated activation of mGluR5 and CB1 promotes neuroprotection.

Edleusa M L Batista, Juliana G Doria, Talita H Ferreira-Vieira, Juliana Alves-Silva, Stephen S G Ferguson, Fabricio A Moreira, Fabiola M Ribeiro

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Edleusa M L BatistaDepartamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Ave. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil.
Juliana G DoriaDepartamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Ave. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil.
Talita H Ferreira-VieiraDepartamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Ave. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil.
Juliana Alves-SilvaDepartamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Ave. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil.
Stephen S G FergusonDepartment of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, K1H8M5, Canada.
Fabricio A MoreiraDepartamento de Farmacologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Fabiola M RibeiroDepartamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Ave. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil. fmribeiro@icb.ufmg.br.
Universidade Federal de Minas Gerais · BRUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabotropic glutamate receptor 5 (mGluR5) and the cannabinoid receptor 1 (CB1) exhibit a functional interaction, as CB1 regulates pre-synaptic glutamate release and mGluR5 activation increases endocannabinoid synthesis at the post-synaptic site. Since both mGluR5 and CB1 promote neuroprotection, we delineated experiments to investigate a possible link between CB1 and mGluR5 activation in the induction of neuroprotection using primary cultured corticostriatal neurons. We find that either the pharmacological blockade or the genetic ablation of either mGluR5 or CB1 can abrogate both CB1- and mGluR5-mediated neuroprotection against glutamate insult. Interestingly, decreased glutamate release and diminished intracellular Ca(2+) do not appear to play a role in CB1 and mGluR5-mediated neuroprotection. Rather, these two receptors work cooperatively to trigger the activation of cell signaling pathways to promote neuronal survival, which involves MEK/ERK1/2 and PI3K/AKT activation. Interestingly, although mGluR5 activation protects postsynaptic terminals and CB1 the presynaptic site, intact signaling of both receptors is required to effectively promote neuronal survival. In conclusion, mGluR5 and CB1 act in concert to activate neuroprotective cell signaling pathways and promote neuronal survival.

Indexed as

NeuroprotectionAnimalsBenzamidesBenzodioxolesCalciumCarbamatesEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesIntracellular SpaceMice, Inbred C57BLModels, BiologicalNeuronsPhosphorylationPiperidinesPresynaptic Terminals3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)benzamideBenzamidesBenzodioxolesCalciumCarbamatescyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterExtracellular Signal-Regulated MAP KinasesJZL 184PiperidinesProto-Oncogene Proteins c-aktPyrazolesReceptor, Cannabinoid, CB1Receptor, Metabotropic Glutamate 5AKTCB1Cell deathERK1/2mGluR5

Identifiers

PMID27543109
PMCPMC4992217
OpenAlexW2514318985

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.