Zinc activates TREK-2 potassium channel activity

J Pharmacol Exp Ther. 2005 Aug;314(2):618-25. doi: 10.1124/jpet.105.084418. Epub 2005 Apr 27.

Abstract

TWIK-related K(+) channel (TREK)-2 is thought to contribute to setting the resting membrane potential and to tuning action potential properties. In the present study, the effects of divalent metal ions (Ba(2+), Co(2+), Ni(2+), Pb(2+), and Zn(2+)) were examined on TREK-2 expressed in Xenopus oocytes using the two-electrode voltage clamping technique. Pb(2+) inhibited TREK channel activity (IC(50) = 15.6 microM), whereas Zn(2+) enhanced it in a dose-dependent manner (EC(50) = 87.1 microM). Ba(2+) slightly inhibited TREK currents but only at high concentrations. Co(2+) and Ni(2+) had no significant effect. The structural element(s) contributing to the zinc enhancement effect were studied using a series of chimeras consisting of Zn(2+)-activated TREK-2 and Zn(2+)-inhibited TWIK-related acid-sensing K(+) channel-3. The structural elements were localized to the first pore and the preceding extracellular loop of TREK-2, in which multiple residues, including His121, His156, Asp158, and Asn177, are likely to be involved in the zinc activation effect. Stimulation by Zn(2+) may be used as a criterion of TREK-2, distinguishing it from other two-pore K(+) channels.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • DNA, Complementary / biosynthesis
  • DNA, Complementary / genetics
  • Dose-Response Relationship, Drug
  • Electrophysiology
  • Extracellular Space / drug effects
  • Extracellular Space / metabolism
  • Humans
  • In Vitro Techniques
  • Lead / pharmacology
  • Membrane Potentials / drug effects
  • Metals / pharmacology
  • Molecular Sequence Data
  • Mutagenesis
  • Mutation / genetics
  • Oocytes / drug effects
  • Oocytes / metabolism
  • Potassium Channel Blockers / pharmacology
  • Potassium Channels / agonists*
  • Potassium Channels / chemistry
  • Potassium Channels / genetics
  • Potassium Channels, Tandem Pore Domain / antagonists & inhibitors
  • Potassium Channels, Tandem Pore Domain / genetics
  • Potassium Channels, Tandem Pore Domain / metabolism
  • Recombinant Fusion Proteins / chemistry
  • Recombinant Fusion Proteins / drug effects
  • Stimulation, Chemical
  • Xenopus
  • Zinc / pharmacology*

Substances

  • DNA, Complementary
  • KCNK10 protein, human
  • KCNK9 protein, human
  • Kcnk10 protein, rat
  • Metals
  • Potassium Channel Blockers
  • Potassium Channels
  • Potassium Channels, Tandem Pore Domain
  • Recombinant Fusion Proteins
  • Lead
  • Zinc