在这里，提出了一个可行的，从来没有调查过的机制，沿神经元的尖峰传播。在下文中，通过不同直径的有髓和无髓轴突的细胞质内部的小振幅压力波的传播速度被理论上估计，并且被发现与动作电位（AP）传导速度大体上一致。这一显著的巧合使得我们可以建立一个模型，在该模型中，AP沿着轴突的传播不是由广泛接受的局部电路理论中的离散离子电流推动的，而是由行进的压力脉冲对膜离子通道的机械激活推动的。计算在粘性轴质中传播的液压脉冲在$\sim$ 1 mm距离上衰减，并且进一步假设，AP Ca $^{2+}$离子期间内流的作用是激活膜骨架蛋白网络进行短暂的径向收缩，放大压力脉冲并防止其衰减。该模型正确地预测，AP传导速度应该随着大的无髓鞘轴突的轴突直径的二分之一功率而变化，并且作为有髓鞘轴突的直径的一次功率，只要轴突的特定机械特性与直径无关;髓鞘化增加传导速度;传导速度随着温度而增加。与局部电路理论不同，该模型能够定性地解释观察到的AP持续时间在较小直径的轴突中的增加。预测…
英文摘要：
Here a viable and never before investigated mechanism of propagation of spikes along neurons is proposed. In the following, velocity of propagation of small-amplitude pressure waves through the cytoplasmic interior of myelinated and unmyelinated axons of different diameters is theoretically estimated, and is found to generally agree with the action potential (AP) conduction velocities. This remarkable coincidence allows to surmise a model in which AP spread along axon is propelled not by straggling ionic currents as in the widely accepted local circuit theory, but by mechanoactivation of the membrane ion channels by a traveling pressure pulse. Hydraulic pulses propagating in the viscous axoplasm are calculated to decay over $\sim$ 1 mm distances, and it is further hypothesized that it is the role of influxing during the AP Ca$^{2+}$ ions to activate the membrane skeletal protein network for a brief radial contraction amplifying the pressure pulse and preventing its decay. The model correctly predicts that the AP conduction velocity should vary as the one-half power of axon diameter for large unmyelinated axons, and as the first power of the diameter for myelinated axons, provided that specific mechanical properties of axons are independent from diameter; that myelinization increases the conduction velocity; that the conduction velocity increases with the temperature. Unlike the local circuit theory, the model is able to qualitatively explain observed increase in the AP duration in axons of smaller diameters. Predictions of...
