CONDUCTION BLOCK BY COCAINE IN SODIUM-DEPLETED NERVES WITH ACTIVITY MAINTAINED BY LITHIUM, HYDRAZINIUM OR GUANIDINIUM IONS

¹ Department of Pharmacology, Seton Hall College of Medicine and Dentistry, Jersey City, New Jersey

The depressant action of cocaine was investigated in sodium-deficient frog peripheral nerves in which excitability was artificially maintained by lithium, hydrazinium or guanidinium ions.

Under these experimental conditions, the action of cocaine was quantitatively affected by the nature of the sodium-substitute. The effect of cocaine was greater in guanidine- and hydrazine-supported nerves than in nerves maintained by sodium or lithium. Also, a mutual antagonism was demonstrated between cocaine and each of the substitutes.

Thus, the cocaine-sensitive excitability mechanism which in normal nerves is intimately associated with sodium, has not been circumvented through the use of the substitute cations. In fact, the cocaine-sodium antagonism is replaced by a cocaine-substitute antagonism emphasizing the competitive antagonism mechanism as the cause of local nerve block by cocaine.