Recovery from C-type inactivation is modulated by extracellular potassium

Biophys J. 1996 Feb;70(2):798-805. doi: 10.1016/S0006-3495(96)79619-4.


Extracellular potassium modulates recovery from C-type inactivation of Kv1.3 in human T lymphocytes. The results of whole-cell patch clamp recordings show that there is a linear increase in recovery rate with increasing [K+]o. An increase from 5 to 150 mM K+o causes a sixfold acceleration of recovery rate at a holding potential of -90 mV. Our results suggest that 1) a low-affinity K+ binding site is involved in recovery, 2) the rate of recovery increases with hyperpolarization, 3) potassium must bind to the channel before inactivation to speed its recovery, and 4) recovery rate depends on external [K+] but not on the magnitude of the driving force through open channels. We present a model in which a bound K+ ion destabilizes the inactivated state to increase the rate of recovery of C-type inactivation, thereby providing a mechanism for autoregulation of K+ channel activity. The ability of K+ to regulate its own conductance may play a role in modulating voltage-dependent immune function.

Publication types

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

MeSH terms

  • Binding Sites
  • Biophysical Phenomena
  • Biophysics
  • Cells, Cultured
  • Extracellular Space / metabolism
  • Humans
  • Kinetics
  • Kv1.3 Potassium Channel
  • Membrane Potentials
  • Potassium / metabolism*
  • Potassium / pharmacology*
  • Potassium Channel Blockers
  • Potassium Channels / drug effects*
  • Potassium Channels / metabolism*
  • Potassium Channels, Voltage-Gated*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism


  • KCNA3 protein, human
  • Kv1.3 Potassium Channel
  • Potassium Channel Blockers
  • Potassium Channels
  • Potassium Channels, Voltage-Gated
  • Potassium