Actin Involvement in Exocytosis from PC12 Cells: Studies on the Influence of Botulinum C2 Toxin on Stimulated Noradrenaline Release
Actin Involvement in Exocytosis from PC12 Cells: Studies on the Influence of Botulinum C2 Toxin on Stimulated Noradrenaline Release
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肌动蛋白参与 PC12 细胞的胞吐作用：肉毒杆菌 C2 毒素对刺激去甲肾上腺素释放影响的研究
DOI：
10.1111/j.1471-4159.1989.tb09131.x
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发表时间：
1989
影响因子：
4.7
通讯作者：
K. Aktories
中科院分区：
文献类型：
--
作者：
Karin Matter;F. Dreyer;K. Aktories
Abstract: Botulinum C2 toxin is known to ADP‐ribosylate actin. The toxin effect was studied on [3H]noradrenaline secretion of PC12 cells. [3H]Noradrenaline release was stimulated five‐ to 15‐fold by carbachol (100 μM) or K+ (50 mM) and 10–30‐fold by the ionophore A23187 (5 μM). Pretreatment of PC12 cells with botulinum C2 toxin for 4–8 h at 20°C, increased carbachol‐, K+‐, and A23187‐induced, but not basal, [3H]noradrenaline release maximally 1.5‐ to threefold, whereas ≥75% of the cellular actin pool was ADP‐ribosylated. Treatment of PC12 cells with botulinum C2 toxin for up to 1 h at 37°C also increased stimulated [3H]noradrenaline secretion, whereas toxin treatment for > 1 h decreased the enhanced [3H]noradrenaline release stimulated by carbachol and K+ but not by A23187. Concomitantly with toxin‐induced stimulation of secretion, 20–50% of the cellular actin was ADP‐ribosylated, whereas >60% of actin was modified when exocytosis was attenuated. The data indicate that ADP‐ribosylation of actin by botulinum C2 toxin largely modulates stimulation of [3H]noradrenaline release. Moreover, the biphasic toxin effects suggest that distinct mechanisms are involved in the role of actin in secretion.
