Abstract：
:Spinal cord injuries alter motor function by disconnecting neural circuits above and below the lesion, rendering sensory inputs a primary source of direct external drive to neuronal networks caudal to the injury. Here, we studied mice lacking functional muscle spindle feedback to determine the role of this sensory channel in gait control and locomotor recovery after spinal cord injury. High-resolution kinematic analysis of intact mutant mice revealed proficient execution in basic locomotor tasks but poor performance in a precision task. After injury, wild-type mice spontaneously recovered basic locomotor function, whereas mice with deficient muscle spindle feedback failed to regain control over the hindlimb on the lesioned side. Virus-mediated tracing demonstrated that mutant mice exhibit defective rearrangements of descending circuits projecting to deprived spinal segments during recovery. Our findings reveal an essential role for muscle spindle feedback in directing basic locomotor recovery and facilitating circuit reorganization after spinal cord injury.
journal_name
Celljournal_title
Cellauthors
Takeoka A,Vollenweider I,Courtine G,Arber Sdoi
10.1016/j.cell.2014.11.019subject
Has Abstractpub_date
2014-12-18 00:00:00pages
1626-39issue
7eissn
0092-8674issn
1097-4172pii
S0092-8674(14)01450-0journal_volume
159pub_type
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