P/Q-type calcium channels activate neighboring calcium-dependent potassium channels in mouse motor nerve terminals

Pflugers Arch. 1997 Aug;434(4):406-12. doi: 10.1007/s004240050414.


The identity of the voltage-dependent calcium channels (VDCC), which trigger the Ca2+-gated K+ currents (IK(Ca)) in mammalian motor nerve terminals, was investigated by means of perineurial recordings. The effects of Ca2+ chelators with different binding kinetics on the activation of IK(Ca) were also examined. The calcium channel blockers of the P/Q family, omega-agatoxin IVA (omega-Aga-IVA) and funnel-web spider toxin (FTX), have been shown to exert a strong blocking effect on IK(Ca). In contrast, nitrendipine and omega-conotoxin GVIA (omega-CgTx) did not affect the Ca2+-activated K+ currents. The intracellular action of the fast Ca2+ buffers BAPTA and DM-BAPTA prevented the activation of the IK(Ca), while the slow Ca2+ buffer EGTA was ineffective at blocking it. These data indicate that P/Q-type VDCC mediate the Ca2+ influx which activates IK(Ca). The spatial association between Ca2+ and Ca2+-gated K+ channels is discussed, on the basis of the differential effects of the fast and slow Ca2+ chelators.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / physiology*
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / physiology*
  • Chelating Agents / pharmacology
  • Egtazic Acid / analogs & derivatives
  • Egtazic Acid / pharmacology
  • Electrophysiology
  • Ion Channel Gating
  • Kinetics
  • Male
  • Mice
  • Motor Neurons / metabolism*
  • Nerve Endings / metabolism*
  • Potassium Channels / drug effects
  • Potassium Channels / physiology*


  • Calcium Channel Blockers
  • Calcium Channels
  • Chelating Agents
  • Potassium Channels
  • 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
  • Egtazic Acid
  • EGTA acetoxymethyl ester
  • Calcium