Analysis of potassium channel functions in mammalian axons by gene knockouts

J Neurocytol. Apr-May 1999;28(4-5):349-64. doi: 10.1023/a:1007013731231.

Abstract

Mammalian axons express a rich repertoire of various K channel subtypes whose distribution is profoundly affected by myelination. In the past two decades, functional analysis of axonal K channels has been approached primarily through pharmacology. Recently, gene knockout techniques have been used to specifically delete a particular K channel subtype from axons. This is significant since the bulk of K channels in a myelinated nerve are covered by the myelin, making functional analysis of specific K channel subtypes by traditional means difficult. This review summarizes the first mutational analysis of this sort performed on an axonal fast K channel termed Kv1.1. This K channel is concealed by the myelin loops in the paranodes of all major myelinated fiber tracts, and exhibits highly heterogeneous distribution even in certain non-myelinated CNS axons. Physiological analysis of Kv1.1 null mutants suggest novel functions for this axonal K channel subtype, including modulation of conduction failures at branch points and stabilization of transition zones in myelinated nerves.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Action Potentials / physiology
  • Animals
  • Axons / chemistry
  • Axons / physiology*
  • Mice
  • Mice, Knockout / physiology*
  • Potassium Channels / genetics*
  • Potassium Channels / metabolism

Substances

  • Potassium Channels