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Transgenic and Mutant Tools to Model Brain Disorders pp 91–112Cite as

Basal Ganglia Disorders in Genetic Models and Experimentally Induced Lesions

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Part of the book series: Neuromethods ((NM,volume 44))

Abstract

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.

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Acknowledgement

This research was funded by a grant from the Natural Sciences and Engineering Research Council of Canada to R.L.

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Authors and Affiliations

  1. Neuroscience Research Unit, University of Montreal/St-Luc, Montreal, QC, Canada

    Robert Lalonde

  2. Faculty of Sciences, University of Rouen, Rouen, France

    Robert Lalonde

  3. Electron Microscopy Service, Faculty of Medicine, University of Nancy I, INSERM U724, Vandoeuvre-les-Nancy, France

    Catherine Strazielle

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  1. Robert Lalonde
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  2. Catherine Strazielle
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Correspondence to Robert Lalonde .

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Editors and Affiliations

  1. School of Medicine, Tulane University, Tulane Ave. 1430, New Orleans, 70112, U.S.A.

    Allan V. Kalueff

  2. E. Pittsburgh Ave. 235, Milwaukee, 53204, U.S.A.

    Carisa L. Bergner

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Lalonde, R., Strazielle, C. (2010). Basal Ganglia Disorders in Genetic Models and Experimentally Induced Lesions. In: Kalueff, A., Bergner, C. (eds) Transgenic and Mutant Tools to Model Brain Disorders. Neuromethods, vol 44. Humana Press. https://doi.org/10.1007/978-1-60761-474-6_5

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  • DOI: https://doi.org/10.1007/978-1-60761-474-6_5

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