Abstract

In 20 adult, unanesthetized spinal cats an attempt has been made to analyze the mechanism by which succinylcholine chloride (Sch) produces fascicular twitching and antidromie motor nerve discharges. Each cat was the subject of repeated, reproducible experiments.

1. Marked increases in afferent discharges of Group la fibers from muscle spindles and in random motoneurone discharges were observed in association with decreases in the amplitude of the monosynaptic reflex of gastrocnemius motoneurones following administration of 20-200 µg/kg of Sch.

2. Fascicular twitching of the gastrocnemius muscle was observed for 1.0-1.5 minutes following 20-30 µg/kg of Sch. It is considered possible that this fascicular twitching may be caused reflexy by increased random motoneurone discharges through partially blocked end-plates.

3. Antidromic motor nerve discharges were obtined from the distal cut end of ventral root filaments in association with the fascicular twitching of the muscle following Sch administration in small doses (20-30 µg/kg). As a possible mechanism by which discharges are elicited, it was suggested that action potentials of muscle fibers elicited by random motoneurone discharges may stimulate motor nerve terminals rendered supersensitive by the drug.

4. Following administration of higher doses of Sch (40-200 µg/kg) it was suggested that twitching and antidromic motor nerve discharges may be attributable to the direct effect of Sch upon motor nerve terminals or muscle fibers. Evidence for this view was derived from the fact that these phenomena were observed even after all the ipsilateral ventral roots caudal to L3 had been cut.

5. Evoked ventral root responses obtained with and without administration of Sch were considered to be attributable to ephaptic conduction phenomena.