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Aconitine-induced increase and decrease of acetylcholine release in the mouse phrenic nerve-hemidiaphragm muscle

M Okazaki1, I Kimura, M Kimura

  • 1Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.

Japanese Journal of Pharmacology
|December 1, 1994
PubMed
Summary
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Aconitine initially boosts acetylcholine release from motor nerves but then inhibits it at higher doses. It also increases spontaneous release, impacting muscle function.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Muscle Physiology

Background:

  • Acetylcholine (ACh) is a key neurotransmitter at the neuromuscular junction.
  • Understanding how toxins affect neurotransmitter release is crucial for neuroscience and toxicology.

Purpose of the Study:

  • To investigate the effects of aconitine on acetylcholine release from motor nerve terminals.
  • To elucidate the mechanisms underlying aconitine's impact on neurotransmission and muscle activity.

Main Methods:

  • Utilized a radioisotope method to measure 3H-ACh release from mouse phrenic nerve-diaphragm preparations.
  • Simultaneously recorded muscle tension alongside evoked and spontaneous 3H-ACh release.
  • Investigated the roles of calcium ions and sodium channels in aconitine's effects, using tetrodotoxin as a control.

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Main Results:

  • Low aconitine concentrations (0.1 microM) increased electrically evoked ACh release.
  • Higher concentrations (0.3-3 microM) decreased evoked release and muscle tension.
  • High concentrations (3-30 microM) increased spontaneous ACh release, with both Ca(2+)-dependent and Ca(2+)-independent components.
  • Aconitine's effects were blocked by tetrodotoxin, indicating involvement of sodium channels.

Conclusions:

  • Aconitine modulates ACh release by prolonged activation and subsequent inactivation of sodium channels in motor nerve terminals.
  • The observed effects on spontaneous release and quantal release depression suggest complex interactions with calcium influx and channel function.
  • Aconitine's dual action on evoked release and its impact on spontaneous release highlight its significant neurotoxic potential.