Two chronic stress models based on movement restriction in rats respond selectively to antidepressant drugs: Aldolase C as a potential biomarker

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dc.contributor.authorAmpuero, Estibaliz
dc.contributor.authorLuarte, Alejandro
dc.contributor.authorSantibañez, Marcos
dc.contributor.authorVaras-Godoy, Manuel
dc.contributor.authorToledo, Jorge
dc.contributor.authorDiaz-Veliz, Gabriela
dc.contributor.authorCavada, Gabriel
dc.contributor.authorJavier Rubio, F.
dc.contributor.authorWyneken, Ursula
dc.date.accessioned2023-03-20T14:09:00Z
dc.date.available2023-03-20T14:09:00Z
dc.date.issued2015-09
dc.descriptionIndexación: Scopuses
dc.description.abstractBackground: Clinically 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. Methods: We 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. Results: We 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. Conclusions: Two 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. © 2015 The Author.es
dc.description.urihttps://academic-oup-com.recursosbiblioteca.unab.cl/ijnp/article/18/10/pyv038/623576
dc.identifier.doi10.1093/ijnp/pyv038
dc.identifier.issn1461-1457
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/47641
dc.language.isoenes
dc.publisherInternational Journal of Neuropsychopharmacology Volume 18, Issue 10September 2015es
dc.rights.licenseAtribución 4.0 Internacional (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectPeripheral Arterial Diseasees
dc.subjectPsychiatric Hospitalses
dc.subjectSerotonin Receptorses
dc.titleTwo chronic stress models based on movement restriction in rats respond selectively to antidepressant drugs: Aldolase C as a potential biomarkeres
dc.typeArtículoes
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