Mode of thyrocalcitonin action in man.
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Biomedical subjects
Publications and source records attributed to H G Haas.
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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.
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The falling phase of action potentials of lobster giant axons is prolonged by DDT; finally a plateau phase is produced like cardiac action potentials. In axons poisoned with DDT, peak transient (sodium) currents associated with step depolarizations are turned off very slowly, and steady-state (potassium) currents are markedly suppressed. These two changes would cause the prolongation of action potentials and are considered the major ionic mechanisms of DDT action.
Saxitoxin at concentrations of 3 x 10(-8) to 3 x 10(-7) mole per liter blocks the conduction of lobster giant axon with no change in resting potential. Recovery of washed axons is faster in those that had been treated with saxitoxin than it is in those that were treated with tetrodotoxin. Peak transient increase in nerve membrane conductance is selectively blocked by saxitoxin with no change in late steady-state increase in conductance. The major mechanism of saxitoxin blockage is the same that of tetrodotoxin blockage.
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