The effects of externally or internally applied morphine hydrochloride on the node of Ranvier of the frog were studied under current and voltage clamp conditions. Externally applied morphine in a concentration of 0.5-1 mM prolonged the action potential and the absolute refractory period. It inhibited the repetitive response of sensory fibres to long-lasting depolarizing pulses. Externally applied morphine was more effective in depressing the steady state K current than the peak Na current. When added to the internal medium (by diffusion from the cut ends of the fibre) morphine had a stronger effect on the peak Na current. Morphine did not alter the kinetics of Na activation but increased the time constants of development or removal of Na inactivation by a factor of about 1.2. Morphine reduced both the fast and slow phase of the inward K tail currents recorded in Ringer with 30 mM K. Of the two components (gKf1 and gKf2) of fast K conductance described by J.M. Dubois (1981, J. Physiol. 318, 297) only gKf2 was affected. The morphine antagonist naloxone in a concentration of 0.1 mM completely and reversibly abolished the component gKf2 of the fast K conductance. Naloxone did not antagonize the effect of morphine. These findings show that there are no specific opiate receptors in the membrane of peripheral nerves.