Motor functions in rat hindlimb muscles following neonatal sciatic nerve crush

Abstract

The sciatic nerve was crushed in the right hindlimb in newborn (3–8 h old) rats. Two to four months later, electromyographic activity was recorded from both the control and reinnervated ankle extensor muscles soleus or lateral gastrocnemius and from the ankle flexor muscle tibialis anterior. Tonic postural activity was present in the extensor muscles on both sides during quiet stance. The control flexor muscles were usually silent in this situation, but the reinnervated flexors exhibited abnormal sustained activity. During locomotion, the control extensors were activated during the stance phase and their mean burst made up 61.5% of the step cycle. The control tibialis anterior muscle fired only during the swing phase, with the burst lasting 18.1% of the step cycle. In the reinnervated extensor muscles, the mean burst duration was decreased (46% of the cycle) but the basic locomotor pattern was not impaired. The reinnervated tibialis muscle, however, was activated abnormally, with one appropriate flexor burst during the swing phase and an “extensor-like” burst during the stance phase of the step. Reflex responses to stretch were weak or absent on the operated side. Histological examination showed that the reinnervated soleus and tibialis muscles were almost devoid of muscle spindles. The motor unit mean firing rates in the reinnervated soleus (22 imp/s) and lateral gastrocnemius (45 imp/s) matched those of the control muscles (25 and 42 imp/s, respectively). In contrast to the phasic, high-frequency firing (52–80 imp/s) in the control tibialis, the reinnervated tibialis motor units fired at significantly lower rates (22–56 imp/s). Thus, neonatal sciatic nerve crush in rats markedly alters the activity pattern in fast flexors, such as the tibialis anterior, whereas the slow (soleus) and fast (lateral gastrocnemius) extensors are much less affected in this respect. The functional changes in the tibialis muscle may reflect increased motoneuron excitability, altered neuronal connectivity and/or lack of inhibition in the spinal cord, as a result of peripheral nerve lesion during a critical developmental period.