Show simple item record

dc.contributor.author Poretti, María Belén
dc.contributor.author Sawant, Rahul S.
dc.contributor.author Rask Andersen, Mathias
dc.contributor.author Fiol, Marta Haydee
dc.contributor.author Schioth, Helgi B.
dc.contributor.author Perez, Mariela Fernanda
dc.contributor.author Carlini, Valeria Paola
dc.date.available 2018-06-28T14:31:40Z
dc.date.issued 2016-03
dc.identifier.citation Poretti, María Belén; Sawant, Rahul S.; Rask Andersen, Mathias; Fiol, Marta Haydee; Schioth, Helgi B.; et al.; Reduced vasopressin receptors activation mediates the anti-depressant effects of fluoxetine and venlafaxine in bulbectomy model of depression; Springer; Psychopharmacology; 233; 6; 3-2016; 1077-1086
dc.identifier.issn 0033-3158
dc.identifier.uri http://hdl.handle.net/11336/50332
dc.description.abstract Rationale: In response to stress, corticotropin releasing hormone (CRH) and vasopressin (AVP) are released from the hypothalamus, activate their receptors (CRHR1, CRHR2 or AVPr1b), and synergistically act to induce adrenocorticotropic hormone (ACTH) release from the anterior pituitary. Overstimulation of this system has been frequently associated with major depression states. Objective: The objective of the study is to assess the role of AVP and CRH receptors in fluoxetine and venlafaxine effects on the expression of depression-related behavior. Methods: In an animal model of depression (olfactory bulbectomy in mice, OB), we evaluated the effects of fluoxetine or venlafaxine (both 10 mg/kg/day) chronic administration on depression-related behavior in the tail suspension test. Plasma levels of AVP, CRH, and ACTH were determined as well as participation of their receptors in the expression of depression related-behavior and gene expression of AVP and CRH receptors (AVPr1b, CRHR1, and CRHR2) in the pituitary gland. Results: The expression of depressive-like behavior in OB animals was reversed by treatment with both antidepressants. Surprisingly, OB-saline mice exhibited increased AVP and ACTH plasma levels, with no alterations in CRH levels when compared to sham mice. Chronic fluoxetine or venlafaxine reversed these effects. In addition, a significant increase only in AVPr1b gene expression was found in OB-saline. Conclusion: The antidepressant therapy used seems to be more likely related to a reduced activation of AVP rather than CRH receptors, since a positive correlation between AVP levels and depressive-like behavior was observed in OB animals. Furthermore, a full restoration of depressive behavior was observed in OB-fluoxetine- or venlafaxine-treated mice only when AVP was centrally administered but not CRH.
dc.format application/pdf
dc.language.iso eng
dc.publisher Springer
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject AVPR1B
dc.subject CORTICOTROPIN RELEASING HORMONE
dc.subject CRHR1
dc.subject DEPRESSIVE BEHAVIOR
dc.subject FLUOXETINE
dc.subject VASOPRESSIN
dc.subject VENLAFAXINE
dc.subject.classification Otras Ciencias Biológicas
dc.subject.classification Ciencias Biológicas
dc.subject.classification CIENCIAS NATURALES Y EXACTAS
dc.title Reduced vasopressin receptors activation mediates the anti-depressant effects of fluoxetine and venlafaxine in bulbectomy model of depression
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2018-06-26T17:18:43Z
dc.identifier.eissn 1432-2072
dc.journal.volume 233
dc.journal.number 6
dc.journal.pagination 1077-1086
dc.journal.pais Alemania
dc.journal.ciudad Berlin
dc.description.fil Fil: Poretti, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
dc.description.fil Fil: Sawant, Rahul S.. Uppsala University. Department of Neuroscience, Functional Pharmacology; Suecia
dc.description.fil Fil: Rask Andersen, Mathias. Uppsala University. Department of Neuroscience, Functional Pharmacology; Suecia
dc.description.fil Fil: Fiol, Marta Haydee. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
dc.description.fil Fil: Schioth, Helgi B.. Uppsala University. Department of Neuroscience, Functional Pharmacology; Suecia
dc.description.fil Fil: Perez, Mariela Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina
dc.description.fil Fil: Carlini, Valeria Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
dc.journal.title Psychopharmacology
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00213-015-4187-4
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00213-015-4187-4
dc.conicet.fuente unificacion


Archivos asociados

Icon
Blocked Acceso no disponible

This item appears in the following Collection(s)

  • Articulos(IFEC) [68]
    Articulos de INST. DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA

Show simple item record

info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)