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Synopsis

Hodgkin and Huxley's theory of nerve-signal conduction was a scientific triumph of the 20th century, but some contradictory experimental findings about nerve signals have been ignored. We currently view the nerve signal as a spike in the resting potential across the cell membrane, which can be modeled as a series of electrical elements containing resistors and capacitors. One then expects some heat dissipation in the components of the system as the pulse passes; yet experiments have shown that the heat initially released at the excitation is reabsorbed by the end of the nerve signal, leading to a net- zero heat generation. With the pulse, currents of ion species move across the membrane and are attributed to the opening and closing of ion-specific channel proteins embedded in the otherwise- impenetrable lipid membrane. But in experiments mimicking physiological conditions, transmembrane currents have also been observed in lipid membranes free of any ion channels. I propose that all these phenomena can be explained by nonequilibrium behavior of the lipid matrix of the cell, which can lead to a new kind of ‘soliton nerve signaling’. This view might help uncover the mode of action of therapies that do not target specific receptors in the nerve membrane, such as general anesthesia and lithium therapy.

Bio: Dana Kamp is a first-year PhD-student in Karel Proesman's group at the Niels Bohr Institute, Copenhagen. She is currently studying optimal control in stochastic non-equilibrium thermodynamics. The work presented is a part of her master's thesis, 'Numerical solutions to the self-contained soliton model – and the potential connection between the soliton theory and lithium treatment in bipolar disorder' from 2021, supervised by Dr. Thomas Heimburg.