English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/97647
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo

AuthorsLlorens-Martín, M. ; Fuster-Matanzo, Almudena ; Teixeira, Catia M.; Jurado-Arjona, Jerónimo ; Ulloa, Fausto; DeFelipe, Javier ; Rábano, Alberto; Hernández Pérez, Félix ; Soriano, Eduardo; Ávila, Jesús
KeywordsGSK-3
Adult hippocampal neurogenesis
Alzheimer’s disease
Post-synaptic density
Environmental enrichment
PSD95
Retrovirus
Issue Date2013
PublisherMacmillan Publishers
CitationMolecular Psychiatry 18: 451- 460 (2013)
AbstractAdult hippocampal neurogenesis (AHN) is crucial for the maintenance of hippocampal function. Several neurodegenerative diseases such as Alzheimer's disease (AD) are accompanied by memory deficits that could be related to alterations in AHN. Here, we took advantage of a conditional mouse model to study the involvement of glycogen synthase kinase-3β (GSK-3β) overexpression (OE) in AHN. By injecting GFP- and PSD95-GFP-expressing retroviruses, we have determined that hippocampal GSK-3β-OE causes dramatic alterations in both dendritic tree morphology and post-synaptic densities in newborn neurons. Alterations in previously damaged neurons were reverted by switching off the transgenic system and also by using a physiological approach (environmental enrichment) to increase hippocampal plasticity. Furthermore, comparative morphometric analysis of granule neurons from patients with AD and from GSK-3β overexpressing mice revealed shared morphological alterations. Taken together, these data indicate that GSK-3β is crucial for hippocampal function, thereby supporting this kinase as a relevant target for the treatment of AD. © 2013 Macmillan Publishers Limited.
URIhttp://hdl.handle.net/10261/97647
DOI10.1038/mp.2013.4
Identifiersdoi: 10.1038/mp.2013.4
issn: 1359-4184
Appears in Collections:(CBM) Artículos
(IC) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.