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.
D Bockenhauer  1 ,  N Zilberberg ,  S A Goldstein
Affiliations
  • 1. Departments of Pediatrics and Cellular and Molecular Physiology, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA.
PMID: 11319556 DOI: 10.1038/87434
Abstract

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.