Abstract
Nicotine has been found to exert a dual action on the end-plate membrane of the frog sartorius muscle. At low concentrations, it decreases the end-plate potential through a suppression of the end-plate sensitivity to acetylcholine without causing marked depolarization, the concentration required to block the end-plate potential by 50% being estimated to be 5 x 10-6 M. Both the sodium and potassium components of the end-plate current are suppressed equally. Continuous perfusion of high concentrations of nicotine causes a transient end-plate depolarization which is followed by a partial repolarization, the concentration required to produce 50% maximum depolarization being estimated to be 6 x 10-5 M. Increases in both sodium and potassium conductances of the end-plate membrane are responsible for the depolarization. During repolarization, the potassium conductance returns to the original resting level, whereas the sodium conductance is only partially inactivated, the residual sodium conductance being responsible for the sustained depolarization. d-Tubocurarine prevents the end-plate depolarization by nicotine. It is concluded that nicotine exerts a dual action on the end-plate membrane at different concentrations by distinctly different mechanisms.
Footnotes
- Received February 22, 1972.
- Accepted May 19, 1972.
- © 1972 by The Williams & Wilkins Co.
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