Maitotoxin activates quantal transmitter release at the neuromuscular junction: evidence for elevated intraterminal Ca2+ in the motor nerve terminal.
Maitotoxin activates quantal transmitter release at the neuromuscular junction: evidence for elevated intraterminal Ca2+ in the motor nerve terminal.
复制标题
麦芽毒素激活神经肌肉接头处的量子递质释放：运动神经末梢末端内 Ca2 升高的证据。
DOI：
10.1016/0006-8993(85)90870-4
复制
发表时间：
1985
期刊：
影响因子：
2.9
通讯作者：
Yasumoto,T
中科院分区：
文献类型：
--
作者：
Kim,YI;Login,IS;Yasumoto,T
美托毒素（MTX），应用于体外小鼠神经肌肉接头，迅速激活乙酰胆碱量子的自发释放，表现为微型终板电位（MEPPs）。这种效应需要外部Ca2+，并伴随着稳定的结后去极化。在自发释放过程的峰值激活之后，量子放电逐渐下降，最终废除MEPP。与MEPP频率的显著增加相反，MTX仅适度增加神经诱发终板电位（EPPs）的量子含量。这些作用归因于毒素提高运动神经末梢中游离细胞内Ca 2+水平的能力。随着其突触前作用位点的进一步表征，maitotoxin可能成为研究突触生理学的有用工具。
Maitotoxin (MTX), applied in vitro to the mouse neuromuscular junction, briskly activates the spontaneous release of acetylcholine quanta, manifest as miniature end-plate potentials (MEPPs). This effect requires external Ca2+and is accompanied by a steady post-junctional depolarization. After the peak activation of the spontaneous release process, the quantal discharge gradually declines with eventual abolishment of MEPPs. In contrast to the striking increase in MEPP frequency, the quantum content of the nerve-evoked end-plate potentials (EPPs) is increased only moderately by MTX. These effects are attributable to the ability of the toxin to elevate the level of free intracellular Ca2+in the motor nerve terminal. With further characterization of its presynaptic site of action, maitotoxin may become a useful tool in studying synaptic physiology.