关于β-银环蛇毒素和响尾蛇毒素对小鼠运动神经末梢乙酰胆碱释放的阻断作用。
On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin.
作者信息
Rowan E G, Pemberton K E, Harvey A L
机构信息
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow.
出版信息
Br J Pharmacol. 1990 Jun;100(2):301-4. doi: 10.1111/j.1476-5381.1990.tb15799.x.
Abstract
- beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.
摘要
- β-银环蛇毒素和响尾蛇毒素是磷脂酶A2神经毒素，它们能不可逆地阻断小鼠胸骨三角肌标本运动神经末梢乙酰胆碱的诱发释放。2. 神经末梢动作电位的细胞外记录显示，递质释放的抑制与动作电位无法侵入神经末梢无关。3. 当诱发递质释放（以细胞内记录的终板电位衡量）被β-银环蛇毒素阻断时，如在对照实验中一样，K⁺诱导的去极化和Ca²⁺离子载体A23187会刺激乙酰胆碱的自发释放。4. 毒素的作用位点尚待阐明，但似乎与动作电位诱导的去极化与释放机制的偶联有关，而非与释放机制本身有关。
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