Basal Ganglia Disorders in Genetic Models and Experimentally Induced Lesions
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Experimentally induced lesions of basal ganglia cause neurological anomalies such as hindlimb clasping and changes in motor activity, together with deficits in motor coordination and spatial learning. Some of these deficits have been described in mice genetically modified for Parkinson’s and Huntington’s disease. Symptoms, similar to those of neurological disorders, are found with lesions of dopaminergic neurons in murine models of Parkinson’s disease, including transgenic mice expressing mutant and wild-type SNCA encoding α-synuclein, Pitx3 -deficient aphakia (ak ) mice, and Park2 null mutants deficient in parkin. As with Huntington’s disease, HD transgenic and knock-in mice with variable CAG repeats have different onsets of anomalies and possess the same time-related biphasic response in motor activity.
