Omega-conotoxin does not block the verapamil-sensitive calcium channels at mouse motor nerve terminals

Neurosci Lett. 1987 Nov 23;82(2):177-80. doi: 10.1016/0304-3940(87)90125-x.

Abstract

Release of acetylcholine at the neuromuscular junctions of skeletal muscle is not sensitive to organic Ca2+ channel blockers. However, in mouse motor nerve endings, extracellular recording reveals that a verapamil-sensitive Ca2+ current can be induced after block of K+ channels. Recordings of extracellular action potentials from inside the perineural sheaths of nerves innervating mouse triangularis sterni muscles reveal that this verapamil-sensitive current is not blocked by omega-conotoxin, and hence, it does not involve channels similar to the L-channels of neuronal cell bodies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anura
  • Calcium / metabolism*
  • Ion Channels / drug effects*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mollusk Venoms / pharmacology*
  • Nerve Block
  • Neuromuscular Junction / metabolism*
  • Verapamil / pharmacology*
  • omega-Conotoxins*

Substances

  • Ion Channels
  • Mollusk Venoms
  • omega-Conotoxins
  • Conus magus toxin
  • Verapamil
  • Calcium