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The Trajectory of Gait Development in Mice

Overview
Journal Brain Behav
Specialty Psychology
Date 2020 Apr 26
PMID 32333523
Citations 22
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Abstract

Objective: Gait irregularities are prevalent in neurodevelopmental disorders (NDDs). However, there is a paucity of information on gait phenotypes in NDD experimental models. This is in part due to the lack of understanding of the normal developmental trajectory of gait maturation in the mouse.

Materials And Methods: Using the DigiGait system, we have developed a quantitative, standardized, and reproducible assay of developmental gait metrics in commonly used mouse strains that can be added to the battery of mouse model phenotyping. With this assay, we characterized the trajectory of gait in the developing C57BL/6J and FVB/AntJ mouse lines.

Results: In both lines, a mature stride consisted of 40% swing and 60% stance in the forelimbs, which mirrors the mature human stride. In C57BL/6J mice, developmental trajectories were observed for stance width, paw overlap distance, braking and propulsion time, rate of stance loading, peak paw area, and metrics of intraindividual variability. In FVB/AntJ mice, developmental trajectories were observed for percent shared stance, paw overlap distance, rate of stance loading, and peak paw area, although in different directions than C57 mice. By accounting for the impact of body length on stride measurements, we demonstrate the importance of considering body length when interpreting gait metrics.

Conclusion: Overall, our results show that aspects of mouse gait development parallel a timeline of normal human gait development, such as the percent of stride that is stance phase and swing phase. This study may be used as a standard reference for developmental gait phenotyping of murine models, such as models of neurodevelopmental disease.

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References
1.
Akula S, McCullough K, Weichselbaum C, Dougherty J, Maloney S . The trajectory of gait development in mice. Brain Behav. 2020; 10(6):e01636. PMC: 7303394. DOI: 10.1002/brb3.1636. View

2.
Schneider T, Skitt Z, Liu Y, Deacon R, Flint J, Karmiloff-Smith A . Anxious, hypoactive phenotype combined with motor deficits in Gtf2ird1 null mouse model relevant to Williams syndrome. Behav Brain Res. 2012; 233(2):458-73. DOI: 10.1016/j.bbr.2012.05.014. View

3.
Dominici N, Ivanenko Y, Cappellini G, dAvella A, Mondi V, Cicchese M . Locomotor primitives in newborn babies and their development. Science. 2011; 334(6058):997-9. DOI: 10.1126/science.1210617. View

4.
Gadalla K, Ross P, Riddell J, Bailey M, Cobb S . Gait analysis in a Mecp2 knockout mouse model of Rett syndrome reveals early-onset and progressive motor deficits. PLoS One. 2014; 9(11):e112889. PMC: 4231076. DOI: 10.1371/journal.pone.0112889. View

5.
Mosconi M, Wang Z, Schmitt L, Tsai P, Sweeney J . The role of cerebellar circuitry alterations in the pathophysiology of autism spectrum disorders. Front Neurosci. 2015; 9:296. PMC: 4555040. DOI: 10.3389/fnins.2015.00296. View