dc.creatorBravo, Javier A.
dc.creatorParra, Claudio S.
dc.creatorArancibia, Sandor
dc.creatorAndrés, Sergio
dc.creatorMorales Retamales, Paola
dc.creatorHerrera-Marschitz Muller, Mario
dc.creatorHerrera, Luisa
dc.creatorLara Peñaloza, Hernán
dc.creatorFiedler Temer, Jenny
dc.date.accessioned2018-12-20T14:11:17Z
dc.date.available2018-12-20T14:11:17Z
dc.date.created2018-12-20T14:11:17Z
dc.date.issued2006
dc.identifierBMC Neuroscience, Volumen 7,
dc.identifier14712202
dc.identifier14712202
dc.identifier10.1186/1471-2202-7-40
dc.identifierhttps://repositorio.uchile.cl/handle/2250/154540
dc.description.abstractBackground: Corticosterone reduction produced by adrenalectomy (ADX) induces apoptosis in dentate gyrus (DG) of the hippocampus, an effect related to an increase in the expression of the pro-apoptotic gene bax. However it has been reported that there is also an increase of the anti-apoptotic gene bcl-2, suggesting the promotion of a neuroprotective phenomenon, perhaps related to the expression of transforming growth factor β1 (TGF-β1). Thus, we have investigated whether TGF-β1 levels are induced by ADX, and whether apoptosis is increased by blocking the expression of TGF-β1 with an antisense oligonucleotide (ASO) administered intracerebrally in corticosterone depleted rats. Results: It was observed an increase of apoptosis in DG, 2 and 5 days after ADX, in agreement with a reduction of corticosterone levels. However, the effect of ADX on the number of apoptotic positive cells in DG was decreased 5 days after the lesion. In CA1-CA3 regions, the effect was only observed 2 days after ADX.
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceBMC Neuroscience
dc.subjectNeuroscience (all)
dc.subjectCellular and Molecular Neuroscience
dc.titleAdrenalectomy promotes a permanent decrease of plasma corticoid levels and a transient increase of apoptosis and the expression of Transforming Growth Factor β1 (TGF-β1) in hippocampus: Effect of a TGF-β1 oligo-antisense
dc.typeArtículos de revistas


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