刺尾鱼毒素在培养的脑干神经元中的钙离子通道激活作用。

Ca2+ channel activating action of maitotoxin in cultured brainstem neurons.

作者信息

Kakizaki Atsushi, Takahashi Masami, Akagi Hiroyuki, Tachikawa Eiichi, Yamamoto Toshifumi, Taira Eiichi, Yamakuni Tohru, Ohizumi Yasushi

机构信息

Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan.

出版信息

Eur J Pharmacol. 2006 May 1;536(3):223-31. doi: 10.1016/j.ejphar.2006.02.052. Epub 2006 Mar 10.

DOI:10.1016/j.ejphar.2006.02.052

PMID:16581067

Abstract

The actions of maitotoxin were studied using cultured brainstem cells and adrenal chromaffin cells. Maitotoxin induced a profound increase in the Ca2+ influx into cultured brainstem cells after a brief lag period. The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem. Maitotoxin-catecholamine release in brainstem cells initiated to increase after a lag period of about 1 min and the increase continued even at 4 min after treatment, while in the adrenal chromaffin cells the release started after an about 1-min lag period to attain a maximum within first 2-min and gradually decrease thereafter. These results suggest that maitotoxin acts on Ca2+ channels to increase the Ca2+ influx, accompanied by enhancement of catecholamine release in the brainstem cells with a different temporal profile from that in the adrenal chromaffin cells.

摘要

利用培养的脑干细胞和肾上腺嗜铬细胞研究了 maitotoxin 的作用。在短暂的延迟期后，maitotoxin 导致培养的脑干细胞中 Ca2+ 内流显著增加。maitotoxin 诱导的 Ca2+ 内流受到各种电压依赖性 Ca2+ 通道阻滞剂（如 Co2+、Mn2+、维拉帕米和地尔硫䓬）的抑制。maitotoxin 诱导的脑干细胞中儿茶酚胺释放约在 1 分钟的延迟期后开始增加，并且在处理后 4 分钟时仍持续增加，而在肾上腺嗜铬细胞中，释放约在 1 分钟的延迟期后开始，在最初 2 分钟内达到最大值，此后逐渐下降。这些结果表明，maitotoxin 作用于 Ca2+ 通道以增加 Ca2+ 内流，同时伴随着脑干细胞中儿茶酚胺释放的增强，其时间模式与肾上腺嗜铬细胞不同。