Introduction

Impulse transmission along a myelinated axon is saltatory, where only the axonal membrane at the nodes of Ranvier is subject to the full action potential. As a consequence of the cytoarchitecture of myelinated nerve, a node of Ranvier can be charged and discharged with a time constant of « 1 ms as its capacity is small (1–2 pF), and its apparent leakage conductance is large (about 20 nS). Delayed rectification is thus not necessary for rapid nodal repolarization. Na+ channel inactivation and the cessation of Na+ ion influx allows rapid repolarization with outward current flow in the leakage pathway. Pharmacological blockade of Xenopus or Rana nodal delayed rectifier with, for example, tetraethylammonium (TEA) ions (Schmidt & Stämpfli, 1966) or extracellular gallamine (Smith & Schauf, 1981; modelled by Frankenhaeuser & Huxley, 1964) causes only a slight prolongation of the action potential (∼0.3 ms at 20 °C). The few rapidly activating K+ channels found at mammalian nodes do not contribute significantly to repolarization (rabbit: Chiu et al., 1979; rat: Brismar, 1980).

The large leakage conductance of the node of Ranvier, as measured in nodal voltage-clamp experiments, is now believed to be part of a current pathway under or through the myelin sheath that allows the internodal axolemma to repolarize the node (Barrett & Barrett, 1982; Blight, 1985; Baker et al., 1987). The movement of charge in this circuit from the node to the internodal capacity during an action potential gives rise to the depolarizing (or negative) after-potential, and an associated phase of increased excitability to applied currents.