Abstract

Sparteine prolongs the falling phase of the nerve action potential. In squid giant axons, the duration is prolonged as much as 100-fold by treatment with 1 x 10^-3 M sparteine, whereas in crayfish giant axons the prolongation is only 2-fold. Resting potential remains unchanged in either preparation. The amplitutde of the action potential is decreased to 65% and 84% in squid and crayfish axons, respectively. In voltage clamped squid axons, potassiunm conductance is suppressed to 67% of the control by 1 x 10^-4 M sparteine and to 12 to 27% of the control by 1 x 10^-3 M sparteine. In sparteine-treated axons, the potassium conductance undergoes a marked inactivation during sustained depolarization which is absent in control preparations. The rate of rise of potassium conductance is slowed, while the time for potassium conductance to reach its half-maximum is shortened. Peak transient sodium conductance is suppressed to 86% and 61% of the control by 1 x 10^-4 and 1 x 10^-3 M sparteine, respectively. Lutanine, a derivative of sparteine, is less potent in prolonging the falling phase of the action potential in crayfish axons. Because of a strong affinity for potassium conductance, sparteine will serve as a useful tool for the study of ionic conductances.