Absence of potassium conductance in central myelinated axons

Abstract

Two voltage-dependent changes in ionic permeability are responsible for the action potential in squid giant axon¹. The depolarization phase of the action potential is due to an initial increase in sodium ion permeability, and repolarization is primarily the result of a later increase in potassium permeability. However, voltage-clamp experiments on mammalian peripheral nodes of Ranvier indicate that potassium conductances (g_k) may be minimal or lacking for intact mammalian peripheral myelinated axons^2–4. Repolarization for these fibres has been explained in terms of a rapid sodium inactivation and large leakage current³. When the myelin around these fibres is acutely disrupted, an immediate and prominent g_k appears⁴. Following demyelination, g_k blocking agents have been shown to reduce late outward currents that are not present in normal myelinated fibres⁵. This suggests that K⁺ channels are present in the axonal membrane under the myelin but are ‘masked’ in normal peripheral myelinated axons. Previous studies have not investigated the presence or role of K⁺ channels in central myelinated axons. We here establish that g_k is not detectable in mammalian dorsal column axons.