Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/43008
Título: 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
Autores/as: 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
Clasificación UNESCO: 320507 Neurología
Palabras clave: Parkinsonism
PINK1
Cannabinoid signaling system
Fecha de publicación: 2009
Editor/a: 0303-6995
Publicación seriada: Journal of Neural Transmission, Supplement 
Resumen: 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
Fuente: Journal of Neural Transmission, Supplementa [ISSN 0303-6995], p. 269-275
Colección:Artículos
Vista completa

Citas SCOPUSTM   

39
actualizado el 24-mar-2024

Visitas

47
actualizado el 17-feb-2024

Google ScholarTM

Verifica

Altmetric


Comparte



Exporta metadatos



Los elementos en ULPGC accedaCRIS están protegidos por derechos de autor con todos los derechos reservados, a menos que se indique lo contrario.