MECHANISM OF THE PARALYSING ACTION OF PIPERAZINE ON ASCARIS MUSCLE

Abstract

The effects of piperazine on Ascaris muscle cells have been investigated with electrophysiological techniques. These cells have an average resting potential of about 30 mV interrupted by rhythmic spikes of myogenic origin (1 to 7 spikes/sec). With piperazine (10⁻³, w/v), the average resting potential increases above 40 mV and the pacemaker activity is suppressed. These changes are similar to those temporarily produced in the same cells by the electrical stimulation of inhibitory nerve fibres. Electrophoretic application of piperazine to different areas of the muscle cells shows that this drug hyperpolarizes their membrane only when applied to the region where both excitatory and inhibitory neuromuscular synapses are located. The degree of muscle hyperpolarization induced by piperazine depends upon the extracellular chloride concentration, decreasing when a fraction of the chloride ions is replaced by the larger, supposedly nonpenetrating, sulphate anions. Piperazine may, therefore, be regarded as a pharmacological analogue of a natural inhibitory transmitter.