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Interaction of DDT with the components of lobster nerve membrane conductance
Abstract:
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.
Insights
The insecticide DDT prolongs the falling phase of nerve action potentials in lobster axons by slowing ion channel closing. This suggests DDT interferes with the normal function of ion channels in nerve membranes.
Area of Science:
- Neuroscience
- Toxicology
- Biophysics
Background:
- Action potentials are crucial for nerve signal transmission.
- Insecticides like DDT can disrupt normal neuronal function.
- Understanding DDT's effects on ion channels is vital for neurotoxicology.
Purpose of the Study:
- To investigate the effects of DDT on the action potential of lobster giant axons.
- To elucidate the specific mechanisms by which DDT alters ion channel kinetics.
- To test the hypothesis of separate ion channels involved in nerve impulse generation.
Main Methods:
- Utilizing voltage-clamp techniques on lobster giant axons.
- Comparing action potential characteristics in control and DDT-treated axons.
- Analyzing current decay kinetics and conductance-voltage relationships.
Main Results:
- DDT markedly prolonged the falling phase of the action potential, introducing a plateau.
- DDT slowed the inactivation (turning-off) of transient sodium currents.
- The maximum peak transient conductance was unaffected, but the decay became multi-exponential.
Conclusions:
- DDT disrupts the normal gating kinetics of ion channels in nerve membranes.
- The findings support a model with at least two distinct ion channel populations.
- DDT's neurotoxic effects are linked to altered ion channel dynamics.