Comparative study of the actions of nicotine and succinylcholine on the monosynaptic reflex and spindle afferent activity

Nicotine, in low doses of 20–40 μg/kg i.v., blocked the monosynaptic reflex without influencing spindle afferent activity. In contrast, succinylcholine depressed the monosynaptic reflex only when it enhanced spindle discharge. Abolition of the spindle excitatory effect of succinylcholine by gallamine or deafferentation eliminated the monosynaptic reflex depressant action of succinylcholine but did not affect that of nicotine. Mecamylamine, on the other hand, which blocks the nicotinic synapse at the Renshaw cell, abolished the monosynaptic reflex blocking effect of nicotine but not that of succinylcholine. These results emphasize the basically different mechanisms underlying the blockade of the monosynaptic reflex by nicotine and succinylcholine.

At intermediate doses of nicotine (40–80 μg/kg i.v.) spindle afferent activity was affected through changes in fusinotor activity consisting of a brief increase followed by prolonged depression. In still higher i.v. doses of nicotine, a direct excitatory effect on the spindle organ was observed. Depression of the monosynaptic reflex through this peripheral effect was revealed when the central action of nicotine was blocked by mecamylamine. Like the action of succinylcholine, it could be blocked by gallamine. Excitation of skin receptors and motor nerve terminals was excluded as a contributory cause of the monosynaptic reflex depression induced by nicotine in the dose range used.