KCNK2: reversible conversion of a hippocampal potassium leak into a voltage-dependent channel

Nat Neurosci. 2001 May;4(5):486-91. doi: 10.1038/87434.


Potassium leak channels are essential to neurophysiological function. Leaks suppress excitability through maintenance of resting membrane potential below the threshold for action potential firing. Conversely, voltage-dependent potassium channels permit excitation because they do not interfere with rise to threshold, and they actively promote recovery and rapid re-firing. Previously attributed to distinct transport pathways, we demonstrate here that phosphorylation of single, native hippocampal and cloned KCNK2 potassium channels produces reversible interconversion between leak and voltage-dependent phenotypes. The findings reveal a pathway for dynamic regulation of excitability.

Publication types

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

MeSH terms

  • Animals
  • Cloning, Molecular
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Electrophysiology
  • Hippocampus / metabolism*
  • Humans
  • Oocytes / metabolism
  • Patch-Clamp Techniques
  • Phenotype
  • Phosphorylation
  • Potassium / metabolism*
  • Potassium Channels / genetics
  • Potassium Channels / metabolism*
  • Potassium Channels, Tandem Pore Domain*
  • Rats
  • Xenopus laevis


  • Potassium Channels
  • Potassium Channels, Tandem Pore Domain
  • potassium channel protein TREK-1
  • Cyclic AMP-Dependent Protein Kinases
  • Potassium