Evidence map›Paper›PMID 25522407›Full record

ArticleThe international journal of neuropsychopharmacology2014

Synaptoproteomic analysis of a rat gene-environment model of depression reveals involvement of energy metabolism and cellular remodeling pathways.

Alessandra Mallei, Marion Failler, Stefano Corna, Giorgio Racagni, Aleksander A Mathé, Maurizio Popoli

Open access · bronzeAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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  7. The dynamics of the stress neuromatrix.Molecular psychiatry · 2016
    Review
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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 2 institutions in 2 countries.

Alessandra MalleiLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé). alessandra.mallei@unimi.it.
Marion FaillerLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Stefano CornaLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Giorgio RacagniLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Aleksander A MathéLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Maurizio PopoliLaboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmacologiche e Biomolecolari and Center of Excellence on Neurodegenerative Diseases, University of Milano, Milano, Italy (Drs Mallei, Failler, Corna, Racagni, and Popoli); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden (Dr Mathé).
Karolinska Institutet · SEUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMajor depression is a severe mental illness that causes heavy social and economic burdens worldwide. A number of studies have shown that interaction between individual genetic vulnerability and environmental risk factors, such as stress, is crucial in psychiatric pathophysiology. In particular, the experience of stressful events in childhood, such as neglect, abuse, or parental loss, was found to increase the risk for development of depression in adult life. Here, to reproduce the gene x environment interaction, we employed an animal model that combines genetic vulnerability with early-life stress.

methodsThe Flinders Sensitive Line rats (FSL), a validated genetic animal model of depression, and the Flinders Resistant Line (FRL) rats, their controls, were subjected to a standard protocol of maternal separation (MS) from postnatal days 2 to 14. A basal comparison between the two lines for the outcome of the environmental manipulation was performed at postnatal day 73, when the rats were into adulthood. We carried out a global proteomic analysis of purified synaptic terminals (synaptosomes), in order to study a subcellular compartment enriched in proteins involved in synaptic function. Two-dimensional gel electrophoresis (2-DE), mass spectrometry, and bioinformatic analysis were used to analyze proteins and related functional networks that were modulated by genetic susceptibility (FSL vs. FRL) or by exposure to early-life stress (FRL + MS vs. FRL and FSL + MS vs. FSL)

resultsWe found that, at a synaptic level, mainly proteins and molecular pathways related to energy metabolism and cellular remodeling were dysregulated.

conclusionsThe present results, in line with previous works, suggest that dysfunction of energy metabolism and cytoskeleton dynamics at a synaptic level could be features of stress-related pathologies, in particular major depression.

Indexed as

Gene-Environment InteractionAge FactorsAnimalsAnimals, NewbornComputational BiologyDepressionDisease Models, AnimalElectrophoresis, Gel, Two-DimensionalEnergy MetabolismMass SpectrometryMaternal DeprivationProteomicsRatsSynaptophysinSynaptosomesSynaptophysinSynpr protein, ratearly-life stressfrontal cortexhippocampusprefrontal cortexproteomicssynaptosome

Identifiers

PMID25522407
PMCPMC4360251
OpenAlexW2112297266

What OpenQuestion holds

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LicenceCC BY-NC
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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.