Hattori T, Maehashi H
Department of Dental Pharmacology, Matsumoto Dental College, Shiojiri, Japan.
Res Commun Chem Pathol Pharmacol. 1992 Feb;75(2):243-6.
We have investigated the interactions between stannous chloride (SnCl2) and calcium (Ca) channel blockers on endplate potentials (e.p.p.) and on miniature endplate potentials (m.e.p.p.) to determine which type of channel (among L-, N-, and T-type) participates in the SnCl2-induced increase in Ca entry into motor nerve terminals. The e.p.p. amplitude augmented by 30 microM SnCl2 was decreased by cumulative addition of 10 microM CdCl2 or 0.5 microM omega-conotoxin but not by 10 microM NiCl2 or 5 microM nicardipine. The SnCl2 (30 microM)-induced rise in m.e.p.p. frequency in high-potassium medium was reduced by 0.5 microM omega-conotoxin but not by 5 microM nicardipine. These results suggest that activation of the N-type Ca channel is involved in the SnCl2-induced increase in Ca entry into the nerve terminals.
我们研究了氯化亚锡(SnCl2)与钙(Ca)通道阻滞剂对终板电位(e.p.p.)和微小终板电位(m.e.p.p.)的相互作用,以确定哪种类型的通道(L型、N型和T型)参与了SnCl2诱导的运动神经末梢钙内流增加。30微摩尔SnCl2增强的e.p.p.幅度,在累积添加10微摩尔CdCl2或0.5微摩尔ω-芋螺毒素后降低,但在添加10微摩尔NiCl2或5微摩尔尼卡地平时未降低。在高钾培养基中,30微摩尔SnCl2诱导的m.e.p.p.频率升高,在添加0.5微摩尔ω-芋螺毒素后降低,但在添加5微摩尔尼卡地平时未降低。这些结果表明,N型钙通道的激活参与了SnCl2诱导的神经末梢钙内流增加。