PRIMARY AFFERENT DEPOLARIZATION AND MONOSYNAPTIC REFLEX DEPRESSION FOLLOWING SUCCINYLCHOLINE ADMINISTRATION

Abstract

The mechanism of monosynaptic reflex response (MSRR) depression produced by the intravenous administration of succinylcholine (SCh) was studied in 75 cats with and without anesthesia. The results and conclusions of this study were as follows: Intravenous SCh in doses of 50-200 [mu]g/kg produces a characteristic depression of both flexor and extensor MSRR''s, an augmentation of polysynaptic reflex responses, and sometimes a random firing of previously quiescent spinal motoneurons. The data shows that the MSRR depression is the direct result of the central actions of afferent impulses evoked by the action of SCh. Reasons are presented for concluding that the reflex depression cannot be adequately explained by inhibition from Group II afferents, recurrent inhibition or post-spike hyperpolarization. The excitability of the intraspinal portions of Group I afferent fibers was found to increase after SCh administration. The time course of the excitability increase was similar to that of the MSRR depression. The excitability increase was attributed to a depolarization of these fibers and was shown to result from the central actions of impulses from the muscle spindle afferents activated peripherally by the SCh. On the basis of the known relationship between afferent fiber depolarization and presynaptic inhibition, it was concluded that the MSRR depression which follows SCh administration results, in part, from augmented presynaptic inhibition.