Behavioural neuroscienceQuantitative measurement of postural sway in mouse models of human neurodegenerative disease
Section snippets
Animals
Transgenic mice (APPSwDI) containing the Swedish, Dutch (E22Q) and Iowa (D23N) amyloid precursor protein (APP) mutations, were generated as described (Davis et al., 2004) and were a generous gift from Dr. William Van Nostrand, Stony Brook University, Stony Brook, NY, USA. P301L mice expressing the P301L human tau mutation were generated as described by Lewis et al. (2000) and were a generous gift from Drs. Lewis and Hutton, Mayo Clinic at Jacksonville, Jacksonville, FL, USA. Bigenic mice were
Results
To verify that body sway could be detected in mice using CoP analysis, we injected young adult (18–25 weeks old), wild type mice with varying doses of harmaline, a known tremorigenic agent. Two concentrations of harmaline were studied using two separate groups of mice (5 mg/kg and 10 mg/kg with five mice per dose) and CoP was performed before treatment, approximately 5 min after induction of tremors and approximately 24 h post-treatment. As shown in Fig. 3, action tremors generated by harmaline
Discussion
Our data demonstrate that CoP analysis provides a simple and quantitative tool to examine motor deficits in pharmacological or genetic mouse models of neurodegenerative diseases. CoP analysis measures postural stability during quiet stance and provides an integrated measure of muscle activity in the inactive (stationary) rodent. Abnormal postural sway in rodents resting on four limbs is likely to represent a mixture of motor deficits; including tremor, imbalance and bradykinesia that each can
Acknowledgments
The authors would like to thank AMTI for their cooperative efforts in designing a suitable mouse CoP platform and for providing the necessary software for analysis.
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