Abstract

Changes in the light scattering signal from single giant axons of lobster were observed during the propagation of the action potential in order to correlate membrane excitability with possible structural changes reflected in the optical properties of the axolemma. Substitution of guanidine and aminoguanidine for sodium resulted in a decreased action potential amplitude to 69 and 50% of control values, respectively. The amplitude of the light signal was, however, not significantly changed by these substitutions and is, therefore, reported to be independent of the transmembrane potential and current. The venom of the scorpion Leiurus quinquestriatus caused a marked prolongation of the action potential and the light scattering signal without significantly altering their amplitudes. A two-state model of the early (sodium) activation channel is suggested, in which the light scattering signal is correlated with a possible difference in the scattering efficiency between the states of the channel.

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