Ochs S, Worth R
Science. 1975 Mar 21;187(4181):1087-9. doi: 10.1126/science.46619.
Batrachotoxin (BTX) irreversibly blocks fast axoplasmic transport in nerve in concentrations as low as 0.2 micromolar. The action of BTX was studied in cat sciatic nerves in vitro by measuring the rate of the crest outflow after injection of the L7 dorsal root ganglion with [3-H]leucine. Tetrodotoxin, which in itself does not affect fast axoplasmic transport, inhibited the blocking action of BTX. Unlike the BTX block of nerve and muscle membrane excitability brought about through increased permeability to sodium ion, the BTX block of fast axoplasmic transport occurs with or without sodium ion in the medium. High concentrations of calcium ion protected against the blocking action of BTX, while magnesium ion did not. An action of BTX on the transport mechanism inside the fibers was indicated by the small reduction of adenosine triphosphate plus creatine phosphate, which in itself did not account for the block of axoplasmic transport.
蛙毒素(BTX)在低至0.2微摩尔的浓度下就能不可逆地阻断神经中的快速轴浆运输。通过测量用[3 - H]亮氨酸注射L7背根神经节后嵴流出的速率,在体外研究了蛙毒素对猫坐骨神经的作用。河豚毒素本身不影响快速轴浆运输,但能抑制蛙毒素的阻断作用。与蛙毒素通过增加对钠离子的通透性导致神经和肌肉膜兴奋性阻断不同,蛙毒素对快速轴浆运输的阻断在培养基中有或没有钠离子的情况下都会发生。高浓度的钙离子可防止蛙毒素的阻断作用,而镁离子则不能。三磷酸腺苷加磷酸肌酸的少量减少表明蛙毒素对纤维内部的运输机制有作用,但其本身并不能解释轴浆运输的阻断。