Soliton model

The Soliton model in neuroscience is a recently developed model that attempts to explain how signals are conducted within neurons. It proposes that the signals travel along the cell's membrane in the form of certain kinds of sound (or density) pulses known as solitons. As such the model presents a direct challenge to the widely accepted Hodgkin-Huxley model which proposes that signals travel as action potentials: voltage-gated ion channels in the membrane open and allow ions to rush into the cell, thereby leading to the opening of other nearby ion channels and thus propagating the signal in an essentially electrical manner.

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History

The Soliton model was developed beginning in 2005 by Thomas Heimburg and Andrew D. Jackson, both at the Niels Bohr Institute of the University of Copenhagen. Heimburg heads the institute's Membrane Biophysics Group and as of early 2007 all published articles on the model come from this group.

Justification

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. It has been known for several decades that an action potential traveling along a neuron results in a slight increase in temperature followed by a decrease in temperature. The decrease is not explained by the Hodgkin-Huxley model (electrical charges traveling through a resistor always produce heat), but traveling solitons do not lose energy in this way and the observed temperature profile is consistent with the Soliton model. Further, it has been observed that a signal traveling along a neuron results in a slight local thickening of the membrane and a force acting outwards; this effect is not explained by the Hodgkin-Huxley model but is clearly consistent with the Soliton model.

It is undeniable that an electrical signal can be observed when an action potential propagates along a neuron. The Soliton model explains this as follows: the traveling soliton locally changes density and thickness of the membrane, and since the membrane contains many charged and polar substances, this will result in an electrical effect, akin to piezoelectricity.

Application

The authors claim that their model explains the previously obscure mode of action of numerous anesthetics. The Meyer-Overton observation holds that the strength of a wide variety of chemically diverse anesthetics is proportional to their lipid solubility, suggesting that they do not act by binding to specific proteins such as ion channels but instead by dissolving in and changing the properties of the lipid membrane. Dissolving substances in the membrane lowers the membrane's freezing point, and the resulting larger difference between body temperature and freezing point inhibits the propagation of solitons. By increasing pressure, lowering pH or lowering temperature, this difference can be restored back to normal, which should cancel the action of anesthetics: this is indeed observed. 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.

See also

• Biological neuron models
• Hodgkin-Huxley model

Sources

• On the (sound) track of anesthetics, press release University of Copenhagen, 6 March 2007
• Kaare Græsbøll. Function of Nerves - Action of Anesthetics, Gamma 143, 2006. An elementary introduction.
• Thomas Heimburg, Andrew D. Jackson. On soliton propagation in biomembranes and nerves. PNAS, vol 102, no. 2. 12 July 2005
• Thomas Heimburg, Andrew D. Jackson. On the action potential as a propagating density pulse and the role of anesthetics. Preprint, October 2006.
• Thomas Heimburg, Andrew D. Jackson. The thermodynamics of general anesthesia. Biophysical Journal, 9 February 2007
• Pradip Das, W. H. Schwarz. Solitons in cell membrane. Physics Review E, 4 November 1994