Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43008
Title: Cannabinoid CB<inf>1</inf> receptors are early DownRegulated followed by a further UpRegulation in the basal Ganglia of mice with deletion of specific park genes
Authors: García-Arencibia, Moisés 
García, Concepción 
Kurz, Alexander
Rodríguez-Navarro, José A.
Gispert-Sánchez, Suzana
Mena, María A.
Auburger, Georg
De Yébenes, Justo García
Fernández-Ruiz, Javier
UNESCO Clasification: 320507 Neurología
Keywords: Parkinsonism
PINK1
Cannabinoid signaling system
Issue Date: 2009
Publisher: 0303-6995
Journal: Journal of Neural Transmission, Supplement 
Abstract: This study was designed to examine the type of changes experienced by the CB1 receptor, a key element of the cannabinoid signaling system, in the basal ganglia of different mouse mutants generated by deletion of specific genes associated with the development of Parkinson's disease in humans [PARK1 (alpha-synuclein), PARK2 (parkin) or PARK6 (PINK1)]. We observed that CB1 receptor-mRNA levels were significantly reduced in the caudate-putamen in the three models under examination when animals were analyzed at early phases (< or = 12 months of age). This decrease was, in general, associated with a reduction in CB1 receptor binding in the substantia nigra and the globus pallidus, particularly in the case of alpha-synuclein-deficient mice. By contrast, both parameters, mRNA levels and binding for the CB1 receptor, showed an elevation in the same areas when animals were analyzed at older ages, mainly in the case of the CB1 receptor binding in the substantia nigra. In summary, our data revealed the existence of a biphasic response for CB1 receptors, with losses at early phases, when dopaminergic dysfunction is possibly the major event that takes place, followed by upregulatory responses at advanced phases characterized by the occurrence of evident nigrostriatal pathology including neuronal death in some cases
URI: http://hdl.handle.net/10553/43008
ISBN: 9783211926598
ISSN: 0303-6995
DOI: 10.1007/978-3-211-92660-4-22
Source: Journal of Neural Transmission, Supplementa [ISSN 0303-6995], p. 269-275
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