Satoh E, Ishii T, Nishimura M
Department of Pharmacology, University of Obihiro School of Veterinary Medicine, Japan.
Jpn J Pharmacol. 2001 Jan;85(1):98-100. doi: 10.1254/jjp.85.98.
The present study was conducted to elucidate the mechanism of the maitotoxin (MTX)-induced increase in intrasynaptosomal free calcium level ([Ca2+]i). The MTX (1 ng/ml)-induced increase in [Ca2+]i was partially inhibited by the omission of extracellular Ca2+ (Ca2+e) or the addition of verapamil, but not by adding nifedipine, omega-agatoxin IVA, omega-conotoxin GVIA and omega-conotoxin MVIIC. An increase in [Ca2+]i in the absence of Ca2+e was sensitive to procaine, TMB-8, genistein and verapamil, but not to ryanodine and U-73122. These results may suggest that MTX increases [Ca2+]i by stimulating Ca2+ entry through voltage-independent nonselective cation channels and Ca2+ release from stores through a phospholipase C-gamma1-mediated pathway in rat cerebrocortical synaptosomes.
本研究旨在阐明刺尾鱼毒素（MTX）诱导突触小体内游离钙水平（[Ca2+]i）升高的机制。MTX（1 ng/ml）诱导的[Ca2+]i升高被细胞外Ca2+（Ca2+e）缺失或维拉帕米的添加部分抑制，但添加硝苯地平、ω-芋螺毒素IVA、ω-芋螺毒素GVIA和ω-芋螺毒素MVIIC则无此作用。在无Ca2+e时[Ca2+]i的升高对普鲁卡因、TMB-8、染料木黄酮和维拉帕米敏感，但对兰尼碱和U-73122不敏感。这些结果可能提示，MTX通过刺激大鼠大脑皮质突触小体中经电压非依赖性非选择性阳离子通道的Ca2+内流以及通过磷脂酶C-γ1介导的途径从储存库释放Ca2+来升高[Ca2+]i。
