1. Intravascular succinylcholine (SCh) administration elicits tonic, irregular discharges of the motoneurones (MN) of cat hindlimb extensor muscles concomitant with activation of their muscle spindle afferents. Stretch of the muscle frequently inhibits the MN-discharges induced by SCh. During maximal spindle activation the monosynaptic massreflex (MMR) is decreased or absent. 2. The administration of dihydro-beta-erythroidine (DHE) prior to SCh abolished the inhibition of MN-discharges induced by muscle stretch. In addition, after DHE the characteristic alternations in groups of MN between discharges and silent periods disappeared. The MMR suppression, induced by SCh, was as a rule reduced or occasionally abolished by DHE pretreatment. 3. Since DHE is known to suppress recurrent Renshaw inhibition, it is suggested that one of the factors responsible for the reflex depressing effect of SCh is an increased recurrent inhibition resulting from increased firing of a fraction of the motoneurones. 4. The existence of DHE resistant MMR depressions after SCh, observed in several cases, indicates that beside recurrent inhibition other factors may be involved.
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