The soma membrane of cat motoneurones was voltage-clamped in vivo using intracellular current and voltage electrodes whose tips were separated by at least 5 μm. Depolarization activates two separate, non-interacting K conductance systems whose rates of activation and decay differ by a factor of about 10. These conductances have a similar reversal potential, in the range of -6 to -21 mV (these and all subsequent voltages are expressed relative to the resting potential). Both conductances show linear 'instantaneous' current-voltage relationships. The steady-state magnitudes of both conductances increase with increasing depolarization. Neither conductance inactivates substantially during prolonged depolarizations. The faster K conductance is similar to that described for squid axons and frog node. Activation begins at about +30 mV and is more than 90% complete within 5 msec of a depolarizing voltage step to +50 mV. Activation kinetics appear to be nonlinear. This fast K conductance contributes to the fast falling phase of the action potential. Following repolarization, this conductance decays with a time constant of 2-4 msec. The slower K conductance activates during depolarizations of 10 mV or greater. The activation and decay of this conductance can be described by first-order exponential functions with time constants ranging from 20 to 50 msec. The slow K conductance underlies the prolonged hyperpolarization that follows motoneurone action potentials. Evidence from other studies suggests that this slow K conductance is regulated by intracellular Ca ions. In addition to the two K conductance systems actiated by depolarization, motoneurones exhibit another distinct conductance system that is activated by hyperpolarization. This third system has a reversal potential near the resting potential. Activation of this conductance during a hyperpolaizing voltage step can be fitted by a single exponential function with a time constant of 50-60 msec over the range -20 to -50 mV. This hyperpolarization-activated conductance accounts for some aspects of the anomalous rectification reported in cat motoneurones. When the clamp circuit was turned off and the motorneurones were stimulated to discharge repetitively by depolarizing current steps, the apparent soma threshold voltage increased as the applied current (and discharge frequency) increased. The basic features of the motoneurone action potential were reconstructed by simulations based on voltage clamp measurements of the voltage dependent conductance systems and previous measurements of passive membrane properties. These simulations assumed that the kinetics of the fast Na and K conductance systems in motoneurons can be described by equations of the same form as the Hodgkin-Huxley equations. These action potential reconstructions indicated that a mjaor portion of the delayed depolarization following the action potential is attributable to capacitative currents from the dendrites. The interspike voltage trajectories measured during low-frequency (primary range) repetitive discharg could be simultated reasonably well by summing the fast and slow K conductances, but during high-frequency (secondary range) discharge simulated trajectories were less depolarized than recorded trajectories.
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