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.
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