Binding of G alpha(o) N terminus is responsible for the voltage-resistant inhibition of alpha(1A) (P/Q-type, Ca(v)2.1) Ca(2+) channels

J Biol Chem. 2001 Aug 3;276(31):28731-8. doi: 10.1074/jbc.M104806200. Epub 2001 Jun 6.

Abstract

G-protein-mediated inhibition of presynaptic voltage-dependent Ca(2+) channels is comprised of voltage-dependent and -resistant components. The former is caused by a direct interaction of Ca(2+) channel alpha(1) subunits with G beta gamma, whereas the latter has not been characterized well. Here, we show that the N terminus of G alpha(o) is critical for the interaction with the C terminus of the alpha(1A) channel subunit, and that the binding induces the voltage-resistant inhibition. An alpha(1A) C-terminal peptide, an antiserum raised against G alpha(o) N terminus, and a G alpha(o) N-terminal peptide all attenuated the voltage-resistant inhibition of alpha(1A) currents. Furthermore, the N terminus of G alpha(o) bound to the C terminus of alpha(1A) in vitro, which was prevented either by the alpha(1A) channel C-terminal or G alpha(o) N-terminal peptide. Although the C-terminal domain of the alpha(1B) channel showed similar ability in the binding with G alpha(o) N terminus, the above mentioned treatments were ineffective in the alpha(1B) channel current. These findings demonstrate that the voltage-resistant inhibition of the P/Q-type, alpha(1A) channel is caused by the interaction between the C-terminal domain of Ca(2+) channel alpha(1A) subunit and the N-terminal region of G alpha(o).

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Binding Sites
  • Brain / metabolism
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels, N-Type / drug effects
  • Calcium Channels, N-Type / physiology*
  • Cattle
  • Female
  • GTP-Binding Protein alpha Subunits, Gi-Go
  • Heterotrimeric GTP-Binding Proteins / chemistry
  • Heterotrimeric GTP-Binding Proteins / metabolism*
  • Kinetics
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Molecular Sequence Data
  • Oocytes / drug effects
  • Oocytes / physiology*
  • Ovary / physiology
  • Peptide Fragments / chemistry
  • Peptide Fragments / metabolism*
  • Peptide Fragments / pharmacology
  • Peptides / chemistry
  • Peptides / metabolism
  • Peptides / pharmacology
  • Protein Subunits
  • Recombinant Fusion Proteins / antagonists & inhibitors
  • Recombinant Fusion Proteins / metabolism
  • Recombinant Proteins / antagonists & inhibitors
  • Recombinant Proteins / metabolism
  • Xenopus laevis

Substances

  • Calcium Channel Blockers
  • Calcium Channels, N-Type
  • Peptide Fragments
  • Peptides
  • Protein Subunits
  • Recombinant Fusion Proteins
  • Recombinant Proteins
  • voltage-dependent calcium channel (P-Q type)
  • GTP-Binding Protein alpha Subunits, Gi-Go
  • Heterotrimeric GTP-Binding Proteins