PMID:15684050

Citation	Perez, FA and Palmiter, RD (2005) Parkin-deficient mice are not a robust model of parkinsonism. Proc. Natl. Acad. Sci. U.S.A. 102:2174-9
Abstract	Mutations in the human parkin gene cause autosomal recessive juvenile parkinsonism, a heritable form of Parkinson's disease (PD). To determine whether mutations in the mouse parkin gene (Park2) also result in a parkinsonian phenotype, we generated mice with a targeted deletion of parkin exon 2. Using an extensive behavioral screen, we evaluated neurological function, motor ability, emotionality, learning, and memory in aged Parkin-deficient mice. The behavioral profile of Parkin-deficient mice on a B6;129S4 genetic background was strikingly similar to that of control mice, and most differences were not reproducible by using coisogenic mice on a 129S4 genetic background. Moreover, catecholamine levels in the striatum, olfactory bulb, and spinal cord of Parkin-deficient mice were normal. In contrast to previous studies using independently generated Parkin-deficient mice, we found no evidence for nigrostriatal, cognitive, or noradrenergic dysfunction. Understanding why Parkin-deficient mice do not exhibit robust signs of parkinsonism could advance knowledge and treatment of PD.
Links	PubMed PMC548311 Online version:10.1073/pnas.0409598102
Keywords	Amphetamines/pharmacology; Animals; Behavior, Animal/physiology; Disease Models, Animal; Emotions; Genotype; Humans; Learning; Memory; Mice; Mice, Inbred C57BL; Mice, Knockout; Motor Activity/drug effects; Motor Activity/physiology; Nerve Tissue/chemistry; Parkinson Disease/genetics; Parkinson Disease/metabolism; Parkinson Disease/physiopathology; Phenotype; Ubiquitin-Protein Ligases/genetics; Ubiquitin-Protein Ligases/metabolism
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