English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/53291
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:


Increased vulnerability to 6-hydroxydopamine lesion and reduced development of dyskinesias in mice lacking CB1 cannabinoid receptors

AuthorsPérez-Rial, Sandra; García-Gutiérrez, María Salud; Molina, José A.; Pérez-Nievas, Beatriz G.; Ledent, Catherine; Leiva, Carlos; Leza, Juan C.; Manzanares, Jorge
Issue Date2011
CitationNeurobiology of Aging 32(4): 631-645 (2011)
AbstractMotor impairment, dopamine (DA) neuronal activity and proenkephalin (PENK) gene expression in the caudate-putamen (CPu) were measured in 6-OHDA-lesioned and treated (l-DOPA. +. benserazide) CB1 KO and WT mice. A lesion induced by 6-OHDA produced more severe motor deterioration in CB1 KO mice accompanied by more loss of DA neurons and increased PENK gene expression in the CPu. Oxidative/nitrosative and neuroinflammatory parameters were estimated in the CPu and cingulate cortex (Cg). CB1 KO mice exhibited higher MDA levels and iNOS protein expression in the CPu and Cg compared to WT mice. Treatment with l-DOPA. +. benserazide (12 weeks) resulted in less severe dyskinesias in CB1 KO than in WT mice.The results revealed that the lack of cannabinoid CB1 receptors increased the severity of motor impairment and DA lesion, and reduced l-DOPA-induced dyskinesias. These results suggest that activation of CB1 receptors offers neuroprotection against dopaminergic lesion and the development of l-DOPA-induced dyskinesias. © 2009 Elsevier Inc.
Identifiersdoi: 10.1016/j.neurobiolaging.2009.03.017
issn: 0197-4580
Appears in Collections:(IN) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
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.