Contribution of cutaneous inputs from the hindpaw to the control of locomotion. II. Spinal cats
- PMID: 12944535
- DOI: 10.1152/jn.00497.2003
Contribution of cutaneous inputs from the hindpaw to the control of locomotion. II. Spinal cats
Abstract
The goal of these experiments was to define the contribution of hindpaw cutaneous inputs in the expression of spinal locomotion in cats. In 3 cats, some (n = 1) or all (n = 2) cutaneous nerves were cut bilaterally at ankle level before spinalization. This denervation caused small deficits that were gradually compensated as reported in the companion study. After spinalization, the completely denervated cats never recovered plantar foot placement or weight bearing of the hindquarters despite more than 35 days of treadmill training. Although normal electromyographic rhythmic activity developed at the hip and knee, ankle flexors and extensors were abnormally coactivated during stance. In contrast, the partially denervated cat regained foot placement and weight support 15 days after spinalization. However, after completing the denervation, foot placement and weight bearing were lost as in previous cats. In a 4th cat, spinalization was performed before denervation and the cutaneous nerves were cut sequentially in the right hindlimb only. Rapid locomotor adaptation occurred after cutting the deep peroneal, saphenous, and sural nerves. Later, cutting the superficial peroneal nerve produced paw drag, which was compensated within 8 days. On cutting the last cutaneous nerve (tibial), plantar foot placement was lost despite another 71 days of training. On the one hand, these experiments show that some cutaneous inputs are necessary for appropriate plantar foot placement and weight bearing of the hindquarters during spinal locomotion and, on the other hand, that locomotor compensation to partial cutaneous denervation after spinalization reveals important adaptive capacities of the spinal cord.
Comment in
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Spinal cord injury reveals unexpected function of cutaneous receptors.J Neurophysiol. 2003 Dec;90(6):3583-4. doi: 10.1152/jn.00839.2003. J Neurophysiol. 2003. PMID: 14665683 No abstract available.
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