Inactivation in Myxicola giant axons responsible for slow and accumulative adaptation phenomena.
1. The action potential in Myxicola giant axons is abolished if the nerve is stimulated at frequencies higher than about 5 sec-1. At 1 sec-1 the magnitude of the action potential is not maintained upon sequential stimulation but decreases until the response is abolished. 2. The behaviour of the ionic currents underlying the action potential was studied with voltage-clamp techniques to find the origin of such adaptation. These studies showed a frequency-dependent decline of the sodium currents. 3. The decline in the Na currents upon repetitive depolarization is shown to be due to a decrease in the Na conductance and not to change in driving force. 4. An analysis of the effects of conditioning depolarizations on the Na current during a depolarizing test pulse demonstrates that in a single short depolarization (less than 10 msec) 15% of the Na conductance enters an inactivated state from which recovery is very slow. Upon repetitive depolarizations the amount of Na conductance available accumulates in this slowly recovering inactivated state. 5. The data are explained by proposing that every time the membrane is depolarized open channels undergo one of two competing reactions. Open channels enter either the traditional inactivated state described by Hodgkin & Huxley (1952b) from which recovery is fast (a few milliseconds) or an inactivated state from which recovery is very slow (seconds). In Myxicola, only 15% of open channels enter the later inactivated state in a single depolarization. Upon repetitive depolarizations, however, the fraction in this state accumulates if the frequency of pulsing is faster than the rate of recovery. 6. Axons in which the amount of open channels entering the slowly recovering inactivated state is significant, such as in Myxicola, have thus a system capable of storing the previous activity of the axon for periods of seconds or minutes.
D000200:Action Potentials; D000222:Adaptation, Physiological; D000818:Animals; D001369:Axons / Q000502:physiology*; D004553:Electric Conductivity; D066298:In Vitro Techniques; D007700:Kinetics; D011077:Polychaeta / Q000502:physiology*; D011188:Potassium / Q000502:physiology; D012964:Sodium / Q000502:physiology
D012964:Sodium; D011188:Potassium