Facilitation of soleus‐coupled Renshaw cells during voluntary contraction of pretibial flexor muscles in man.

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102

SUMMARY1. I a projections and recurrent inhibition from quadriceps to tibialis anterior and soleus motoneurones were investigated in man.2. Changes in the firing probability of individual voluntarily activated motor units were studied following electrical stimulation of the femoral nerve or quadriceps tendon tap.3. Femoral nerve stimulation evoked an early increase in the firing probability of tibialis anterior units. This excitation was also evoked by a tendon tap, had a low threshold and its central delay was estimated to be the same as that of the homonymous monosynaptic Ia excitation. These findings strongly suggest that the femoral nerve-induced excitation is I a in origin and mediated through a monosynaptic pathway.4. The frequency of heteronymous Ia excitation from quadriceps was about the same to both ankle flexor and extensor units (79 and 70 % respectively).5. In 80 % of both tibialis anterior and soleus units the I a excitation was followed by a decrease in firing probability. This inhibition had a short latency and a long duration (up to 40 ms); it always appeared with the quadriceps reflex discharge and increased with it. These findings suggest that this decrease in firing probability is due to the Renshaw inhibition evoked by the quadriceps motoneurone discharge.6. Both the Ia excitation and the following inhibition of tibialis anterior and soleus units were also observed when the stimulation was applied to the nerve of the vastus lateralis (a pure knee extensor).7. The functional significance of these identical projections from quadriceps to both ankle flexor and extensor motoneurones is discussed with regard to the requirements of bipedal stance and gait.

Section: Discussionmentioning

confidence: 99%

Monosynaptic Ia excitation and recurrent inhibition from quadriceps to ankle flexors and extensors in man.

Meunier

Pénicaud

Pierrot-Deseilligny

et al. 1990

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102

“…In humans, characteristic changes in recurrent inhibition have been observed during various voluntary and postural contractions: (1) weak tonic contraction of triceps surae, quadriceps and pretibial flexors increases the excitability of the respective Renshaw cells more than can be explained by the input from active motor axon collaterals (Hultborn & Pierrot-Deseilligny, 1979;Rossi & Mazzocchio, 1991), whereas strong tonic contraction of triceps surae decreases the excitability of Renshaw cells which can only be explained by a simultaneous inhibitory convergence on the Renshaw cells (Hultborn & PierrotDeseilligny, 1979); (2) before and at the beginning of phasic ramp contractions of triceps surae there is some indication of Renshaw cell facilitation which shifts progressively to an inhibition that peaks at the end of the ramp (Katz, Pierrot-Deseilligny & Hultborn, 1982); (3) tonic or phasic ramp contractions of the pretibial flexors increase the recurrent inhibition of soleus motoneurones (Katz & Pierrot-Deseilligny, 1984); (4) postural contractions while standing unsupported (Pierrot-Deseilligny, Morin, Katz & Bussel, 1977) and after backward tilt of the head-body (Rossi, Mazzocchio & Scarpini, 1987) increase the excitability of Renshaw cells projecting to soleus motoneurones. From all these studies it appears that various supraspinal inputs can modify transmission in the recurrent pathway during natural movements.…”

mentioning

confidence: 99%

Depression of Renshaw recurrent inhibition by activation of corticospinal fibres in human upper and lower limb.

Mazzocchio

Rossi

Rothwell

1994

1. This study tested whether the recurrent inhibition of soleus and wrist flexor motoneurones could be modified by transcranial magnetic stimulation in human subjects. 2. Magnetic stimulation was given through a circular coil centred at the vertex. The intensity of the magnetic stimulus was subthreshold for evoking a motor response in the active soleus and wrist flexor muscles. The recurrent inhibition brought about by a conditioning H1 reflex discharge was estimated by a test H' reflex. The modifications of the recurrent inhibition after cortical stimulation were distinguished from the motoneuronal changes by comparing H' to a reference H reflex. 3. In the soleus motoneurones, the reference H reflex was inhibited at a minimum conditioning‐test interval of ‐2 ms (H reflex stimulus before magnetic stimulation). In contrast, the H' reflex was facilitated at minimum conditioning‐test intervals of +1 ms. In the wrist flexor motoneurones, both H' and reference H reflexes were facilitated. However, at lower cortical stimulus intensities, only the H' reflex was facilitated at minimum conditioning‐test intervals of +1 ms. 4. In both motoneurone pools, H' facilitation started 3‐4 ms later than the earliest changes in the reference H reflex. Also, the threshold of H' facilitation was lower than that of reference H reflex. 5. It is concluded that facilitation of the H' reflex is produced by corticospinal inhibition of Renshaw cells via a short interneuronal chain in both the upper and lower limb.

“…In fact, two arguments point against the alternative possibility that the control of soleus-coupled Renshaw cells during co-contraction is only the net result of the effects observed during isolated voluntary plantar and dorsiflexion. Firstly, the net result of the large facilitation of the H' reflex observed during strong plantar flexion (Hultborn & Pierrot-Deseilligny, 1979; see also Figs 1 and 2) and of the moderate inhibition observed during strong dorsiflexion (Katz & Pierrot-Deseilligny, 1984, their Figs 1 and 2) could very unlikely be the strong inhibition constantly observed here during strong co-contraction (Fig. 2C).…”

Section: Discussionmentioning

confidence: 99%

“…Since the reference H reflex decreased with dorsiflexion, there was no significant difference in the two reflexes during this task (P > 0 1), although the H' reflex was marginally more depressed than the reference H reflex (AH' -AHref = -0 6). As already discussed in detail by A F Hultborn & Pierrot-Deseilligny (1979) and Katz & Pierrot-Deseilligny (1984), neither the different sensitivity to preand postsynaptic inhibition of reference and H' reflexes, nor the stimulation of afferent fibres by the conditioning stimulation can account for the significantly smaller size of the H' than of the reference H reflex during weak plantar flexion and co-contraction. This must therefore reflect an increased recurrent inhibition from the Hi conditioning reflex during the two tasks.…”

mentioning

confidence: 89%

Evidence of facilitation of soleus‐coupled Renshaw cells during voluntary co‐contraction of antagonistic ankle muscles in man.

Nielsen

Pierrot-Deseilligny

1996

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1. The amount of recurrent inhibition onto soleus motoneurones was compared during plantar flexion and co-contraction of antagonistic ankle plantar and dorsiflexors at matched levels of background activity in the soleus muscle. 2. During weak plantar flexion and co-contraction (less than 10% of maximal voluntary plantar flexion effort) a test reflex discharge (H' reflex), which was conditioned by a previous reflex discharge, was found to be significantly more depressed in relation to rest than an unconditioned reference H reflex. During strong plantar flexion (more than 50 % of maximal voluntary plantar flexion effort) the H' reflex either increased more or to the same extent as the reference H reflex in relation to rest. In contrast to this, the H' reflex was strongly depressed during co-contraction, whereas the reference H reflex was not significantly different from its resting value. 3. At the end of the ramp phase of a phasic contraction, large variations of the H' reflex were observed during plantar flexion (large increase in relation to rest) and during co-contraction (marked decrease), whereas the reference H reflex was facilitated in the two situations. 4. These observations provide evidence that soleus-coupled Renshaw cells are differently regulated during co-contraction and plantar flexion. It is suggested that the Renshaw cells are inhibited during strong plantar flexion but not during strong co-contraction. The functional significance of the findings is discussed.