Morphine and the synaptic activation of Renshaw cells

Abstract

Morphine administered electrophoretically prolonged the latencies of action potentials of Renshaw cells evoked by maximal and submaximal stimulation of ventral roots, without reducing the sensitivity of these neurones to electrophoretically administered acetylcholine. Such an effect was not observed when spikes were evoked by dorsal root stimuli, suggesting that morphine impairs the release of acetylcholine from motoneurone axon collaterals. High concentrations of morphine had a direct excitant action on Renshaw cells, and a procaine-like effect on action potentials and the sensitivity to both acetylcholine and dl-homocysteate. Morphine administered i.v. in doses (10 mg/kg) which substantially reduce the recurrent inhibition of motoneurones did not alter the latencies of Renshaw cell firing in response to submaximal ventral root stimuli. The effect of the alkaloid on the recurrent inhibition of spinal motoneurones occurs predominantly at Renshaw cell-motoneurone inhibitory synapses.