Evidence map›Paper›PMID 25813018›Full record

ArticleThe international journal of neuropsychopharmacology2015

Two Chronic Stress Models Based on Movement Restriction in Rats Respond Selectively to Antidepressant Drugs: Aldolase C As a Potential Biomarker.

Estibaliz Ampuero, Alejandro Luarte, Marcos Santibañez, Manuel Varas-Godoy, Jorge Toledo, Gabriela Diaz-Veliz, Gabriel Cavada, F Javier Rubio, Ursula Wyneken

Open access · goldAbstract readComparative Study
In one paragraph

Article in The international journal of neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Adulthood effects of developmental exercise in rats.Developmental psychobiology · 2024
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  19. BioMed research international · 2019
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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

9 authors at 3 institutions in 1 country.

Estibaliz AmpueroFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Alejandro LuarteFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Marcos SantibañezFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Manuel Varas-GodoyFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Jorge ToledoFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Gabriela Diaz-VelizFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Gabriel CavadaFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
F Javier RubioFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy).
Ursula WynekenFacultad de Medicina, Universidad de los Andes, Chile (Dr Ampuero, Mr Luarte, Dr Santibañez, Mr Toledo, Drs Varas-Godoy, Cavada, Rubio, and Wyneken); Laboratorio de Neurobiologia, Centro de Investigaciones Biomedicas, Universidad Andres Bello, Santiago, Chile (Dr Ampuero); Facultad de Medicina, Universidad de Chile (Dr Diaz-Veliz); Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (Dr Varas-Godoy). uwyneken@uandes.cl.
Universidad Andrés Bello · CLUniversidad de Los Andes, Chile · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinically depressed individuals respond to different types of antidepressants, suggesting that different neurobiological mechanisms may be responsible for their depression. However, animal models to characterize this are not yet available.

methodsWe induced depressive-like behaviors in rats using 2 different chronic stress models: restraint in small cages or immobilization in adaptable plastic cones. Both models increased anxiety responses evaluated by novelty-suppressed feeding and the elevated plus-maze; increased learned helplessness evaluated by the tail suspension and forced swimming tests; and increased anhedonia evaluated by the sucrose preference test.

resultsWe assessed the ability of 2 different types of antidepressants to ameliorate depressive-like behaviors. We administered the serotonin reuptake inhibitor fluoxetine or the noradrenaline reuptake inhibitor reboxetine once daily for 28 days to rats that received either chronic restraint or immobilization stress, or no stress. Behavioral analysis revealed that fluoxetine ameliorated depressive-like behaviors when induced by chronic restraint stress, whereas reboxetine ameliorated these behaviors when induced by chronic immobilization stress. To further test biological differences between both models, we evaluated the levels of Aldolase C, an enzyme expressed by forebrain astrocytes that is regulated by antidepressant treatment, in the cerebrospinal fluid: chronic restraint stress, but not immobilization stress, increased the levels of Aldolase C. Moreover, the presence of astrocyte-derived Aldolase C-GFP in the cerebrospinal fluid indicates its central origin.

conclusionsTwo stress paradigms induced depressive-like behaviors that were sensitive to different antidepressant treatments. Biomarkers such as Aldolase C could help determine optimal antidepressant treatments for clinically depressed patients.

Indexed as

AnimalsAntidepressive AgentsChronic DiseaseDepressive DisorderDisease Models, AnimalFluoxetineFructose-Bisphosphate AldolaseGreen Fluorescent ProteinsMaleMorpholinesRats, Sprague-DawleyReboxetineRestraint, PhysicalSelective Serotonin Reuptake InhibitorsSerotonin and Noradrenaline Reuptake InhibitorsStress, PsychologicalAntidepressive AgentsFluoxetineFructose-Bisphosphate AldolaseGreen Fluorescent ProteinsMorpholinesReboxetineSelective Serotonin Reuptake InhibitorsSerotonin and Noradrenaline Reuptake Inhibitorschronic stressFluoxetineimmobilizationreboxetinerestraint

Identifiers

PMID25813018
PMCPMC4648154
OpenAlexW2093926960

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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.