DOES d-TUBOCURARINE INHIBIT THE RELEASE OF ACETYLCHOLINE FROM MOTOR NERVE ENDINGS?

Abstract

The effect of d-tubocurarine on the release of ACh from guinea pig phrenic nerve-diaphragm preparations was reinvestigated at high frequency of stimulations (50 cps). Various types of anticholinesterases, including DFP, Mipafox, Echothiophate and neostigmine, were used as cholinesterase inhibitors. The results show that in no case d-tubocurarine appeared to reduce the ACh release. Thus, our result confirms the earlier finding of DALE et al.(1936) but is contradictory to that of BEANI et al.(1964) although essentially similar procedure was followed. In contrast, Hemicholinium-3 reduced the ACh output to less than 20 per cent of control levels. Nerve terminal spikes of rat diaphragm preparations recorded with extracellular microelectrodes were not affected by d-tubocurarine whether with single or repetitive stimulations. The size of successive end-plate potentials evoked by repetitive stimulation at 100 cps in the preparation treated with Hemicholinium-3 declined more rapidly than that of curarized muscle. It is concluded that d-tubocurarine does not influence the presynaptic event of neuromuscular transmission even at high frequency of stimulation and that the Wedensky inhibition in curarized muscles is not due to a pharmacological effect of d-tubocurarine.