Abstract
Experiments on nerves in situ and on isolated nerves provide no evidence that morphine interferes with impulse transmission in myelinated or nonmyelinated nerve fibres. The concentrations used in experiments on isolated nerves were 10- to 100-times as high as those required to depress transmission at autonomic nerve-effector cell junctions. Examination of the resting membrane potential, the action potential and the positive after-potential, the conduction velocity, the time courses of the recovery of the size of the action potential and of the excitability after a conditioning stimulus, the ability of the axons to sustain repetitive activity and the posttetanic hyperpolarization gave no indication that morphine affects either the mechanisms involved in the initiation of the propagated impulse or those leading to restoration of the resting state after activity. Analgesic drugs, such as pethidine and methadone which have a local anaesthetic action, may cause a reversible decrease in the size of the compound action potential and in the conduction velocity of A-B and C fibres.