We studied the potential contribution of postsynaptic mechanisms to the depression of reflex excitability which occurs immediately after a voluntary release from tonic muscle contraction. The excitability of the Soleus (Sol) motor pool was tested at rest and after voluntary muscle relaxation. In both cases the Sol H-reflex was conditioned by a single shock to the peroneal nerve, in order to activate the Ia interneurones (INs) mediating the reciprocal inhibition via a peripheral input, or by a short-lasting voluntary contraction of the Tibialis Anterior (TA) muscle, to activate the Ia INs via a central command. Changes in excitability of Renshaw cells were also tested at rest and after release, to assess the role of recurrent inhibition in the release-induced inhibition of the Sol H-reflex. It was demonstrated that: the excitability of the INs mediating the reciprocal inhibition was only slightly enhanced in comparison with resting conditions; the H-reflex of the antagonist muscle (TA) evoked after Sol release was not consistently facilitated with respect to rest; the command to contract the TA muscle reduced the H-reflex of the Sol muscle during rest but not after Sol release; recurrent inhibition did not increase its effect in the post-release period. Such features suggest that recurrent and reciprocal post-synaptic inhibitions do not play a major role in reducing the reflex excitability of a relaxing muscle; rather, the command to release prevents the reciprocal inhibitory effect which accompanies the contraction of the antagonist muscle.

Excitability of reciprocal and recurrent inhibitory pathways after voluntary muscle relaxation in man.

SCHIEPPATI, MARCO;
1985-01-01

Abstract

We studied the potential contribution of postsynaptic mechanisms to the depression of reflex excitability which occurs immediately after a voluntary release from tonic muscle contraction. The excitability of the Soleus (Sol) motor pool was tested at rest and after voluntary muscle relaxation. In both cases the Sol H-reflex was conditioned by a single shock to the peroneal nerve, in order to activate the Ia interneurones (INs) mediating the reciprocal inhibition via a peripheral input, or by a short-lasting voluntary contraction of the Tibialis Anterior (TA) muscle, to activate the Ia INs via a central command. Changes in excitability of Renshaw cells were also tested at rest and after release, to assess the role of recurrent inhibition in the release-induced inhibition of the Sol H-reflex. It was demonstrated that: the excitability of the INs mediating the reciprocal inhibition was only slightly enhanced in comparison with resting conditions; the H-reflex of the antagonist muscle (TA) evoked after Sol release was not consistently facilitated with respect to rest; the command to contract the TA muscle reduced the H-reflex of the Sol muscle during rest but not after Sol release; recurrent inhibition did not increase its effect in the post-release period. Such features suggest that recurrent and reciprocal post-synaptic inhibitions do not play a major role in reducing the reflex excitability of a relaxing muscle; rather, the command to release prevents the reciprocal inhibitory effect which accompanies the contraction of the antagonist muscle.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/117704
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