  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...
