The neuroprotective agent riluzole activates the two P domain K(+) channels TREK-1 and TRAAK

Mol Pharmacol. 2000 May;57(5):906-12.

Abstract

Riluzole (RP 54274) is a potent neuroprotective agent with anticonvulsant, sedative, and anti-ischemic properties. It is currently used in the treatment of amyotrophic lateral sclerosis. This article reports that riluzole is an activator of TREK-1 and TRAAK, two important members of a new structural family of mammalian background K(+) channels with four transmembrane domains and two pore regions. Whereas riluzole activation of TRAAK is sustained, activation of TREK-1 is transient and is followed by an inhibition. The inhibitory process is attributable to an increase of the intracellular cAMP concentration by riluzole that produces a protein kinase A-dependent inhibition of TREK-1. Mutants of TREK-1 lacking the Ser residue where the kinase A phosphorylation takes place are activated in a sustained manner by riluzole. TRAAK is permanently activated by riluzole because, unlike TREK-1, it lacks the negative regulation by cAMP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COS Cells
  • Cyclic AMP / metabolism
  • Neuroprotective Agents / pharmacology*
  • Potassium Channels / chemistry
  • Potassium Channels / drug effects
  • Potassium Channels / metabolism*
  • Potassium Channels, Tandem Pore Domain*
  • Protein Structure, Tertiary / drug effects
  • Riluzole / pharmacology*
  • Transfection

Substances

  • Neuroprotective Agents
  • Potassium Channels
  • Potassium Channels, Tandem Pore Domain
  • potassium channel protein TREK-1
  • Riluzole
  • Cyclic AMP