Further insight into the regulation of Renshaw cell activity

Summary Changes in the excitability of the soleus H-reflex arc were reduced in all the cases in which the recurrent inhibition at rest was normal, while such a reduction was never observed studied after oral administration of L-acetylcarnitine, a in the patients in whom recurrent inhibition was found to be cholinomimetic substance, in eight healthy control subjects decreased at rest. In the former cases, the size of the H 9 and 23 spastic patients presenting with slowly progressive reflex evoked by the same conditioning H1 discharge was paraparesis (n 5 10), a cord lesion (n 5 9) and a cerebral further depressed after L-acetylcarnitine, pointing to a lesion (n 5 4). Changes in the amount of recurrent inhibition potentiating effect of the drug on Renshaw cells; in the latter of soleus motor neurons at rest were also estimated in order cases no such effect was seen. A significant decrease in the to assess the level of activity of Renshaw cells before and mean Hmax :M max ratio after L-acetylcarnitine intake was after L-acetylcarnitine administration. Recurrent inhibition also seen in the healthy control subjects. Possible changes elicited by a conditioning reflex discharge (H1) was assessed in the amount of presynaptic inhibition on Ia terminals on by a subsequent test reflex (H9). Four patients lacked an H9 soleus motor neurons afterL-acetylcarnitine were ruled out. reflex. In ~50% of the remaining patients, recurrent inhibition It is proposed that the differential effect of the drug on the was normal, while in the other half there was evidence of H-reflex excitability is directly related to the level of Renshaw reduced or absent inhibitory activity at rest. Pooling the data cell activity, a reduction of which probably follows a lesion relative to the effect of L-acetylcarnitine on the H-reflex in interrupting reticulo-spinal pathways with tonic facilitatory relation to the strength of recurrent inhibition disclosed that influences on Renshaw cells. These findings support the the ratio of peak-to-peak amplitude values of the maximum hypothesis that Renshaw cell excitability is set via corticoreticulo-spinal systems. H reflex to maximum M wave responses (H max :M max) was