Effects of verapamil on the sustained depolarization of rat diaphragm myocyte pretreated with neostigmine or 3,4-diaminopyridine
- VernacularTitle:维拉帕米对新斯的明或3,4-二氨基吡啶引起的大鼠膈肌持续性去极化的作用(英)
- Author:
Lijun LI
;
Chuangui LIU
- Publication Type:Journal Article
- Keywords:
diaphragm;
neuromuscular junction;
calcium channels;
endplate potential;
sustained depolarization;
verapamil;
neostigmine;
3,4-diaminopyridine
- From:
Chinese Journal of Pharmacology and Toxicology
2002;16(1):1-7
- CountryChina
- Language:Chinese
-
Abstract:
AIM To study the effects of verapamil on end-plate potentials(EPPs) in isolated non-uniform stretched muscle preparation(INSMP) of rat diaphragms pretreated with neostigmine or 3,4-diaminopyridine(3,4-DAP). METHODS Using conventional intracellular microelectrode recording technique. RESULTS A sustained depolarization could be induced at the end-plate area pre-incubated with 0.2－5.0 μmol·L-1 neostigmine or 1.0－4.0 mmol·L-1 3,4-DAP. In normal Tyrode solution, verapamil at a concentration of 1, 5, 10 or 20 μmol·L-1 had no significant effect on evoked endplate potentials and miniature endplate potentials. However, the sustained depolarization due to neostigmine or 3,4-DAP could be antagonized by verapamil at 5－20 μmol·L-1 and the duration of the depolarization was shortened in a concentration-dependent manner. CONCLUSIONL-type calcium ion channels can be activated by accumulated acetylcholine in the synaptic cleft and may be involved in producing sustained depolarization, while they play no role in transmitter release under normal physiological conditions.
