Evidence map›Paper›PMID 27581816›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2018

Altered expression of schizophrenia-related genes in mice lacking mGlu5 receptors.

Alessia Luoni, Peter Gass, Paolo Brambilla, Mirella Ruggeri, Marco A Riva, Dragos Inta

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Article in European archives of psychiatry and clinical neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 9 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

6 authors at 5 institutions in 3 countries.

Alessia LuoniDepartment of Pharmacological and Biomolecular Sciences, Center of Neuropharmacology, Università degli Studi di Milano, Milan, Italy.
Peter GassDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health Mannheim, Medical Faculty Mannheim, University of Heidelberg, J 5, 68159, Mannheim, Germany.
Paolo BrambillaDepartment of Neurosciences and Mental Health, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy.
Mirella RuggeriSection of Psychiatry, Department of Neurological, Biomedical and Movement Sciences, University of Verona, Verona, Italy.
Marco A RivaDepartment of Pharmacological and Biomolecular Sciences, Center of Neuropharmacology, Università degli Studi di Milano, Milan, Italy.
Dragos IntaDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health Mannheim, Medical Faculty Mannheim, University of Heidelberg, J 5, 68159, Mannheim, Germany. Dragos.Inta@zi-mannheim.de.
University of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITUniversity Hospital Heidelberg · DEUniversity of Basel · CHUniversity of Verona · IT

Funding

Deutsche Forschungsgemeinschaft IN-168/3-1Ministero della Salute GET UP Project Code H61J08000200001
6 · The paper itself

Abstract

The evidence underlying the so-called glutamatergic hypothesis ranges from NMDA receptor hypofunction to an imbalance between excitatory and inhibitory circuits in specific brain structures. Among all glutamatergic system components, metabotropic receptors play a main role in regulating neuronal excitability and synaptic plasticity. Here, we investigated, using qRT-PCR and western blot, consequences in the hippocampus and prefrontal/frontal cortex (PFC/FC) of mice with a genetic deletion of the metabotropic glutamate receptor 5 (mGlu5), addressing key components of the GABAergic and glutamatergic systems. We found that mGlu5 knockout (KO) mice showed a significant reduction of reelin, GAD65, GAD67 and parvalbumin mRNA levels, which is specific for the PFC/FC, and that is paralleled by a significant reduction of protein levels in male KO mice. We next analyzed the main NMDA and AMPA receptor subunits, namely GluN1, GluN2A, GluN2B and GluA1, and we found that mGlu5 deletion determined a significant reduction of their mRNA levels, also within the hippocampus, with differences between the two genders. Our data suggest that neurochemical abnormalities impinging the glutamatergic and GABAergic systems may be responsible for the behavioral phenotype associated with mGlu5 KO animals and point to the close interaction of these molecular players for the development of neuropsychiatric disorders such as schizophrenia. These data could contribute to a better understanding of the involvement of mGlu5 alterations in the molecular imbalance between excitation and inhibition underlying the emergence of a schizophrenic-like phenotype and to understand the potential of mGlu5 modulators in reversing the deficits characterizing the schizophrenic pathology.

Indexed as

AnimalsBrainCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsFemaleGene Expression RegulationGlutamate DecarboxylaseMaleMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsParvalbuminsProtein SubunitsReceptor, Metabotropic Glutamate 5Receptors, Ionotropic GlutamateCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsGlutamate Decarboxylaseglutamate decarboxylase 1glutamate decarboxylase 2Nerve Tissue ProteinsParvalbuminsProtein SubunitsReceptor, Metabotropic Glutamate 5Receptors, Ionotropic GlutamateReelin ProteinReln protein, mouseRNA, MessengerSerine EndopeptidasesGABAergic systemGlutamate receptorsMiceReelinSchizophrenia

Identifiers

PMID27581816
OpenAlexW2512553079

What OpenQuestion holds

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Registered trials

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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.