Nakanishi A, Yoshizumi M, Morita K, Murakumo Y, Houchi H, Oka M
Department of Pharmacology, Tokushima University School of Medicine, Japan.
Neurosci Lett. 1991 Jan 2;121(1-2):163-5. doi: 10.1016/0304-3940(91)90675-j.
The effect of palytoxin (PTX), a potent marine toxin, on catecholamine release from cultured bovine adrenal chromaffin cells was examined. PTX at concentrations of over 10(-9) M induced catecholamine release dose-dependently. About 40-50% of the total cellular catecholamine was released during 20-min incubation with 3 x 10(-8) M PTX. PTX-induced catecholamine release was dependent on both extracellular Na+ and Ca2+, and was inhibited by organic and inorganic Ca2+ channel blockers, but not by tetrodotoxin. PTX-induced increase in 45Ca2+ influx into the cells, which was associated with catecholamine release, was also inhibited by these Ca2+ channel blockers. These results indicated that PTX-induced catecholamine release was mediated by activation of Na(+)-dependent, tetrodotoxin (TTX) insensitive voltage-dependent Ca2+ channels.
研究了强效海洋毒素岩沙海葵毒素（PTX）对培养的牛肾上腺嗜铬细胞释放儿茶酚胺的影响。浓度超过10^(-9) M的PTX可剂量依赖性地诱导儿茶酚胺释放。在与3×10^(-8) M PTX孵育20分钟期间，约40 - 50%的细胞内总儿茶酚胺被释放。PTX诱导的儿茶酚胺释放依赖于细胞外的Na+和Ca2+，并受到有机和无机Ca2+通道阻滞剂的抑制，但不受河豚毒素的抑制。这些Ca2+通道阻滞剂也抑制了PTX诱导的45Ca2+流入细胞，这与儿茶酚胺释放有关。这些结果表明，PTX诱导的儿茶酚胺释放是由Na(+)依赖性、对河豚毒素（TTX）不敏感的电压依赖性Ca2+通道的激活介导的。
