Worth R M, Ochs S
J Neurobiol. 1982 Nov;13(6):537-49. doi: 10.1002/neu.480130608.
Batrachotoxin (BTX) in the low concentration range of 19-190 nM blocks axoplasmic transport in the desheathed cat peroneal nerve in vitro. When the level of Na+ in the incubation medium was reduced to 10 mM, the blocking effect of BTX was much diminished, and in an Na+-free medium BTX had no effect on transport at all. The blocking action of BTX with Na+ present was inhibited by increasing the concentration of Ca2+ in the experimental medium. Relatively small increases were effective with a maximum protection seen when the Ca2+ concentrations were 7-10 mM. The results support the view that an increase in axonal Na+ is inhibitory to the transport mechanism. The results are discussed on the basis of the recently developed transport filament model of axoplasmic transport which takes into account an obligatory role for Ca2+ in transport and its axonal regulation. The possible relation of intraaxonal Na+ concentration to the Ca2+ level is also discussed.
浓度在19 - 190纳摩尔范围内的蛙毒素(BTX)在体外可阻断去鞘猫腓神经中的轴浆运输。当孵育培养基中的Na⁺水平降至10毫摩尔时,BTX的阻断作用大大减弱,而在无Na⁺培养基中,BTX对运输完全没有影响。实验培养基中Ca²⁺浓度的增加可抑制BTX在有Na⁺存在时的阻断作用。相对较小的增加就有效,当Ca²⁺浓度为7 - 10毫摩尔时可看到最大程度的保护。这些结果支持轴突Na⁺增加对运输机制有抑制作用这一观点。基于最近发展的轴浆运输细丝模型对结果进行了讨论,该模型考虑了Ca²⁺在运输及其轴突调节中的必要作用。还讨论了轴突内Na⁺浓度与Ca²⁺水平的可能关系。