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1 Physiology, University of Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: trevor.drew{at}umontreal.ca.
We used microwire electrodes chronically implanted into the hindlimb representation of the motor cortex as well as into the pyramidal tract to test the hypothesis that the corticospinal system contributes to the locomotor plasticity that is observed following cutaneous denervation of the cat hindpaw. A total of 23 electrodes implanted into the motor cortex in 3 cats trained to walk on a treadmill produced phase-dependent, short-latency, twitch responses in hindlimb flexor and extensor muscles during locomotion. Following a unilateral cutaneous denervation of the hindpaw, the cats showed transient deficits in locomotion, including a dragging of the hindpaw along the treadmill belt during the swing phase. This deficit rapidly recovered over the course of a few days. The recovery of locomotion was accompanied by an increase in the magnitude of the responses evoked in different muscles by the cortical stimulation at all 23 cortical sites. Response magnitude increased rapidly within the first 1-2 weeks post-denervation before attaining a plateau at
3 weeks. In 2 cats, for which detailed information was obtained, response magnitude in the knee flexor, semitendinosus (St), was increased by > 250% at 14/18 sites (mean increase = 1235% ). Increased responses in the St to stimulation were also observed at 2/4 of the pyramidal tract sites following the denervation but were relatively smaller (max = 593%) than those evoked by the cortical stimulation. We suggest that the denervation produces changes in both cortical and spinal excitability that, together, produce a change in corticospinal efficacy that contributes to the recovery of locomotor function.
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