title: 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 axon. 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 (gk) may be minimal or lacking for intact mammalian peripheral myelinated axons. Repolarization for these fibres has been explained in terms of a rapid sodium inactivation and large leakage current. When the myelin around these fibres is acutely disrupted, an immediate and prominent gk appears. Following demyelination, gk blocking agents have been shown to reduce late outward currents that are not present in normal myelinated fibres. 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 gk is not detectable in mammalian dorsal column axons.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D004553:Electric Conductivity; D009413:Nerve Fibers, Myelinated / Q000502:physiology*; D011188:Potassium / Q000502:physiology*; D051381:Rats; D013116:Spinal Cord / Q000502:physiology*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
chemical_list: D000631:Aminopyridines; D013757:Tetraethylammonium Compounds; D011188:Potassium