Abstract
Movement disorders observed following peripheral nerve injury and muscle reinnervation suggest discoordination in the activation of antagonist muscles. Although underlying mechanisms remain undecided, dysfunction in spinal reflex circuits is a reasonable candidate. Based on the well known role of reflex inhibition between agonist and antagonist muscles in normal animals, we hypothesized its reduction following muscle reinnervation, similar to that associated with other disorders exhibiting antagonist discoordination, e.g. spinal cord injury and dystonia. Experiments performed on acutely-decerebrated rats examined interactions of mechanosensory reflexes between ipsilateral muscles acting as mechanical antagonists at the ankle joint: ankle extensor, gastrocnemii (G) muscles (agonists) and ankle flexor, tibialis anterior (TA) muscle (antagonist). The force of agonist stretch reflex contraction was measured for its suppression or facilitation by concurrent conditioning stretch of the antagonist muscle. Data were compared between two groups of adult rats, an antagonist reinnervation group with TA muscle reinnervated and a control group with TA normally innervated. Results revealed a three-fold increase in reflex suppression in the antagonist reinnervation group, contrary to our predicted decrease. Reflex facilitation also increased, not only in strength, seven-fold, but also in its frequency of stochastic occurrence across stimulus trials. These observations suggest dysregulation in specific spinal reflex circuits as novel candidate origins of modified antagonist muscle coordination following peripheral nerve injury and muscle reinnervation.