Evidence map›Paper›PMID 36230976›Full record

ArticleCells2022

The Neuroprotective Effects of mGlu1 Receptor Antagonists Are Mediated by an Enhancement of GABAergic Synaptic Transmission via a Presynaptic CB1 Receptor Mechanism.

Elisa Landucci, Rolando Berlinguer-Palmini, Gilda Baccini, Francesca Boscia, Elisabetta Gerace, Guido Mannaioni, Domenico E Pellegrini-Giampietro

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 4 institutions in 3 countries.

Elisa LanducciDepartment of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, 50139 Florence, Italy.ORCID 0000-0002-6776-2857
Rolando Berlinguer-PalminiThe BioImaging Unit, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne NE2 4HH, UK.ORCID 0000-0002-1786-496X
Gilda BacciniInstitute of Physiology, Christian-Albrechts-University Kiel, 24118 Kiel, Germany.
Francesca BosciaDepartment of Neuroscience, Division of Pharmacology, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0003-1572-0484
Elisabetta GeraceDepartment of Neuroscience, Psychology, Drug Research and Child Health (NeuroFarBa), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.ORCID 0000-0001-8448-6092
Guido MannaioniDepartment of Neuroscience, Psychology, Drug Research and Child Health (NeuroFarBa), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.ORCID 0000-0002-8273-7377
Domenico E Pellegrini-GiampietroDepartment of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, 50139 Florence, Italy.ORCID 0000-0002-3920-2297
University of Florence · ITChristian-Albrechts-Universität zu Kiel · DENewcastle University · GBUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we investigated the cross-talk between mGlu1 and CB1 receptors in modulating GABA hippocampal output in whole-cell voltage clamp recordings in rat hippocampal acute slices, in organotypic hippocampal slices exposed to oxygen and glucose deprivation (OGD) and in gerbils subjected to global ischemia. CB1 receptor expression was studied using immunohistochemistry and the CA1 contents of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were measured by LC-MS/MS. Our results show that mGlu1 receptor antagonists enhance sIPSCs in CA1 pyramidal cells and the basal and ischemic hippocampal release of GABA in vivo in a manner that is mediated by CB1 receptor activation. In hippocampal slices exposed to OGD and in ischemic gerbils, mGlu1 receptor antagonists protected CA1 pyramidal cells against post-ischemic injury and this effect was reduced by CB1 receptor activation. OGD induced a transient increase in the hippocampal content of AEA and this effect is prevented by mGlu1 receptor antagonist. Finally, OGD induced a late disruption of CB1 receptors in the CA1 region and the effect was prevented when CA1 pyramidal cells were protected by mGlu1 antagonists. Altogether, these results suggest a cooperative interaction between mGlu1 receptors and the endocannabinoid system in the mechanisms that lead to post-ischemic neuronal death.

Indexed as

EndocannabinoidsNeuroprotective AgentsAnimalsChromatography, LiquidExcitatory Amino Acid Antagonistsgamma-Aminobutyric AcidGerbillinaeGlucoseOxygenRatsReceptor, Cannabinoid, CB1Receptors, PresynapticSynaptic TransmissionTandem Mass SpectrometryEndocannabinoidsExcitatory Amino Acid Antagonistsgamma-Aminobutyric AcidGlucoseNeuroprotective AgentsOxygenReceptor, Cannabinoid, CB1Receptors, Presynaptic2-methyl-6-(phenylethynyl)pyridine (MPEP)cannabinoidshippocampusinhibitory post synaptic current (IPSC)ischemiamGluR(S)-3,5-dihydroxyphenylglycine (DHPG)(S)-(+)-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385)

Identifiers

PMID36230976
PMCPMC9562021
OpenAlexW4297348635

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.