Soliton model in neuroscience

The soliton hypothesis in neuroscience is a model that claims to explain how action potentials are initiated and conducted along axons based on a thermodynamic theory of nerve pulse propagation.

Soliton hypothesis proponents assert that energy is mainly conserved during propagation except dissipation losses; Measured temperature changes are completely inconsistent with the Hodgkin-Huxley model.

The measurement of a temperature pulse and the claimed absence of heat release during an action potential[5][6] were the basis of the proposal that nerve impulses are an adiabatic phenomenon much like sound waves.

Based on Tasaki's work, Konrad Kaufman proposed sound waves as a physical basis for nerve pulse propagation in an unpublished manuscript.

[11] The basic idea at the core of the soliton model is the balancing of intrinsic dispersion of the two dimensional sound waves in the membrane by nonlinear elastic properties near a phase transition.

[12] Solitons are the simplest solution of the set of nonlinear wave equations governing such phenomenon and were applied to model nerve impulse in 2005 by Thomas Heimburg and Andrew D. Jackson,[13][14][15] both at the Niels Bohr Institute of the University of Copenhagen.

The biological physics group of Matthias Schneider has studied propagation of two-dimensional sound waves in lipid interfaces and their possible role in biological signalling [16][17][18][19] The model starts with the observation that cell membranes always have a freezing point (the temperature below which the consistency changes from fluid to gel-like) only slightly below the organism's body temperature, and this allows for the propagation of solitons.

[9] In addition, the action potential causes a slight local thickening of the membrane and a force acting outwards;[21] this effect is not predicted by the Hodgkin–Huxley model but does not contradict it, either.

Indeed, such nonlinear sound waves have now been shown to exist at lipid interfaces that show superficial similarity to action potentials (electro-opto-mechanical coupling, velocities, biphasic pulse shape, threshold for excitation etc.).

The amount of pressure needed to cancel the action of an anesthetic of a given lipid solubility can be computed from the soliton model and agrees reasonably well with experimental observations.