The recurrent inhibition of monosynaptic reflexes and its alteration after peripheral nerve crush in decerebrate rats
In decerebrate rats, recurrent inhibition between lateral gastrocnemius-soleus (LG-S) and medial gastrocnemius (MG) motor pools was assessed by conditioning monosynaptic reflexes elicited from the cut dorsal roots and recorded either from the LG-S and MG nerves by antidromic volleys delivered to the synergist muscle nerve. The results show that following sciatic nerve crush in both experimental groups there is a significant sustained depression in the level of recurrent inhibition. The reduction in recurrent inhibition observed is less in adult animals when comparisons are made with the results from rats given the nerve injury early in postnatal life. However, following lateral gastrocnemius-soleus nerve crush instead of sciatic nerve crush, which shortened the dennervation time respectively, the reduction of recurrent inhibition was not observed in adult rat group and was much less in 5-day-old rat group. In addition, the different contributions of the recurrent inhibition between LG-S and MG motor pools are dedifferentiated as a result of nerve injury. It is proposed that this reduction of recurrent inhibition occurs due to degeneration of motor axon collaterals following the nerve injury. Such degeneration has been observed in the cat following axotomy (Havton & Kellerth, 1984, 1990a). The maintained reduction of recurrent inhibition may therefore be a consequence of a failure of regenerating axon collaterals to re-establish contact with Renshaw cells and/or alterations in the membrane properties of the injured motoneurones. However, this kind of degeneration may not occur if dennervation is short enough. In conclusion, this observed reduction of recurrent inhibition may contribute to the hyperreflexia reported in young animals following nerve crush (Navarrete et al., 1990) and that the results in this study support the view that peripheral nerve injury induces plastic changes in the behaviour of spinal circuitry.