Locomotor gaits depend on the interplay between distributed spinal neural networks termed central pattern generators generating rhythmic and coordinated movements, primary afferents and descending supraspinal inputs. Recent studies demonstrated that the mouse display a rich repertoire of locomotor gaits. Changes in locomotor gaits occur in mutant mice lacking particular neurons or molecular signaling pathways implicated in the normal establishment of these neural networks Given the role of the Down Syndrome Cell Adherence Molecule (DSCAM) to the formation and maintenance of spinal interneuronal circuits and sensorimotor integration, we have investigated its functional contribution to locomotor gaits over a wide range of locomotor speeds using freely walking mice. We show here that the DSCAM2J mutation, while not precluding any gait, impairs the age- and speed-dependent modulation of locomotor gaits. It impairs the ability of mice to maintain their locomotion at high treadmill speeds. DSCAM2J mutation induces the dominance of lateral walk over trot and the emergence of aberrant gaits for mice, such as pace and diagonal walk. Locomotor gaits were also more labile in DSCAM2J mutant mice, i.e. less stable, less attractive and less predictable than their wild-type littermates. Our results suggest that the DSCAM mutation affects the behavioral repertoire of gaits in an age- and speed-dependent manner.
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