Following transaction and surgical repair of a muscle nerve in the cat, motor and sensory axons gradually reinnervate the muscle over the course of 6-9 months, but the sensory information is permanently blocked from accessing the parent muscle. It has been shown in patients that such nerve injuries result in permanent loss of dexterity, suggesting an important role for sensory feedback from muscles in motor coordination. In previous cycles of this program project, it was shown that one year after animals received transection and repair of the nerves to the triceps surae muscles the animals exhibited a loss of ankle joint stiffness that resulted in a pronounced ankle joint yield when the animals walked down a ramp but not up the ramp. These findings are consistent with the directional properties of length feedback. In the last grant cycle, it was found that the pronounced yield following reinnervation was absent or much reduced if the animals underwent treadmill training for 12 months following the transection and repair, even though the stretch reflex remained absent. We now propose three new investigations. The first is to elucidate the manner in which the animal was able to compensate for the loss of directionally-specific feedback. Second, we plan to investigate the possibility that systematic training on ramp walking itself might provide a means of restoring local feedback to muscles. Third, we wish to understand the contributions of a second receptor, the Golgi tendon organ that provides force-related feedback to muscles in the limb. We will address these questions using a combination of experiments and computer simulations. Experiments in the cat will be used to address the mechanisms underlying adaptations to the loss of muscle force and sensory feedback. Computer simulations will be used to understand how peripheral nerve injury and adaptations to this injury result in changes in global coordination of the joints of the limb. Finally, we will use ramp training in an attempt to restore local sensory feedback. These experiments will test the extent to which an animal can use an alternative pattern of muscle recruitment to compensate for the deficits from peripheral nerve injuries and provide additional insight into the specific roles of sensory information from muscle spindles and Golgi tendon organs. Finally, we will attempt to employ a therapy to restore the normal mechanisms of motor coordination.
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