Studies on neuromuscular blockade by boldine in the mouse phrenic nerve-diaphragm

Jaw Jou Kang, Yu Wen Cheng, Wen Mei Fu

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The effects of boldine [(S)-2,9-dihydroxyl-1,10-dimethoxy-aporphine], a major alkaloid in the leaves and bark of Boldo (Peumus boldus Mol.), on neuromuscular transmission were studied using a muscle phrenic-nerve diaphragm preparation. Boldine at concentrations lower than 200 μM preferentially inhibited, after an initial period of twitch augmentation, the nerve-evoked twitches of the mouse diaphragm and left the muscle-evoked twitches unaffected. The twitch inhibition could be restored by neostigmine or washout with Krebs solution. The twitches evoked indirectly and directly were both augmented initially, suggesting that the twitch augmentation induced by boldine was myogenic. Boldine inhibited the acetylcholine-induced contraction of denervated diaphragm dose-dependently with an IC50 value of 13.5 μM. At 50 μM, boldine specifically inhibited the amplitude of the miniature end plate potential. In addition, boldine was similar to d-tubocurarine in its action to reverse the neuromuscular blocking action of α-bungarotoxin. These results showed that the neuromuscular blockade by boldine on isolated mouse phrenic-nerve diaphragm might be due to its direct interaction with the postsynaptic nicotinic acetylcholine receptor.

Original languageEnglish
Pages (from-to)207-212
Number of pages6
JournalJapanese Journal of Pharmacology
Volume76
Issue number2
DOIs
Publication statusPublished - Feb 1998
Externally publishedYes

Keywords

  • Acetylcholine channel
  • Boldine
  • Neuromuscular blockade
  • Peumus boldus Mol.

ASJC Scopus subject areas

  • Pharmacology
  • Molecular Medicine

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