  It is suggested that the propagation of the action potential is accompanied
by an axoplasmic pressure pulse propagating in the axoplasm along the axon
length. The pressure pulse stretch-modulates voltage-gated Na (Nav) channels
embedded in the axon membrane, causing their accelerated activation and
inactivation and increasing peak channel conductance. As a result, the action
potential propagates due to mechano-electrical activation of Nav channels by
straggling ionic currents and the axoplasmic pressure pulse. The velocity of
such propagation is higher than in the classical purely electrical Nav
activation mechanism, and it may be close to the velocity of propagation of
pressure pulses in the axoplasm. Extracellular Ca ions influxing during the
voltage spike, or Ca ions released from intracellular stores, may trigger a
mechanism that generates and augments the pressure pulse, thus opposing its
viscous decay. The model can potentially explain a number of phenomena that are
not contained within the purely electrical Hodgkin-Huxley-type framework: the
Meyer-Overton rule for the effectiveness of anesthetics, as well as various
mechanical, optical and thermodynamic phenomena accompanying the action
potential. It is shown that the velocity of propagation of axoplasmic pressure
pulses is close to the measured velocity of the nerve impulse, both in absolute
magnitude and in dependence on axon diameter, degree of myelination and
temperature.
