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Recurrent inhibition to soleus motoneurones, brought about by a conditioning H-reflex discharge, was estimated in human subjects by a subsequent test H reflex. Changes in recurrent inhibition during voluntary ankle dorsiflexion were evaluated by comparing the amplitude of the test H reflex to a reference H reflex: both reflexes were subjected to the same type of influences which modified soleus monosynaptic reflex excitability during pretibial flexor contraction, but only the test H reflex was subject to the recurrent inhibition evoked by the conditioning H-reflex discharge. During tonic or phasic ramp contractions of the pretibial flexors the inhibition of the test H reflex, as compared to rest, was more marked than that of the reference H reflex. Evidence is presented that this may indicate a facilitation of soleus-coupled Renshaw cells. Since this facilitation of soleus-coupled Renshaw cells was also observed before ramp contraction, it is, at least in part, supraspinal in origin. Within the range of forces studied (8-45% of maximum force) there was no evidence that the facilitation of soleus-coupled Renshaw cells increased along with increased force of the pretibial flexor voluntary contraction. During voluntary phasic ankle dorsiflexion, facilitation of soleus-coupled Renshaw cells was maximum at the moment when soleus motoneurones were most facilitated by the stretch-induced soleus I a discharge. There was no evidence for changes in Renshaw cell excitability during ballistic contractions. It is suggested that this facilitation of soleus-coupled Renshaw cells may be one of the mechanisms preventing the occurrence of a soleus stretch reflex during a voluntary ankle dorsiflexion. Such a mechanism could become important if reciprocal inhibition, via I a inhibitory interneurones, were not strong enough, e.g. because of a weak gamma-drive to the contracting muscles.

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				J. F. Iles and J. Pardoe Changes in transmission in the pathway of heteronymous spinal recurrent inhibition from soleus to quadriceps motor neurons during movement in man Brain, September 1, 1999; 122(9): 1757 - 1764. [Abstract] [Full Text] [PDF]