Interaction of DDT with the components of lobster nerve membrane conductance.
The falling phase of action potential of lobster giant axons is markedly prolonged by treatment with DDT, and a plateau phase appears as in cardiac action potentials. Repetitive afterdischarge is very often superimposed on the plateau. Voltage-clamp experiments with the axons treated with DDT and with DDT plus tetrodotoxin or saxitoxin have revealed the following: DDT markedly slows the turning-off process of peak transient current and suppresses the steady-state current. The falling phase of the peak transient current in the DDT-poisoned axon is no longer expressed by a single exponential function as in normal axons, but by two or more exponential functions with much longer time constants. The maximum peak transient conductance is not significantly affected by DDT. DDT did not induce a shift of the curve relating the peak transient conductance to membrane potential along the potential axis. The time to peak transient current and the time for the steady-state current to reach its half-maximum are prolonged by DDT to a small extent. The finding that, under the influence of DDT, the steady-state current starts flowing while the peak transient current is partially maintained supports the hypothesis of two operationally separate ion channels in the nerve membrane.
D000200:Action Potentials; D000818:Animals; D001369:Axons; D002462:Cell Membrane; D003445:Crustacea; D003634:DDT / Q000494:pharmacology*; D004731:Endotoxins / Q000494:pharmacology; D008564:Membrane Potentials; D009431:Neural Conduction / Q000187:drug effects*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D004731:Endotoxins; D013779:Tetrodotoxin; D003634:DDT