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Nerve soliton (转载)

已有 4386 次阅读 2009-3-16 22:20 |个人分类:光孤子理论|系统分类:科研笔记| Nerve, signals, may, shock, wave

Nerve signals may be shock wave riders:

Wired has a good break down of theory that says that nerve cells don't work on electricity as we assume, but instead transmit signals using pressure waves, and crucially, this might explain how anaesthetics work.

The idea that nerve cells send their signals as pressure waves is not brand new. Known as the Soliton model, it was first published in 2005 by Drs Andrew Jackson and Thomas Heimburg and was thought a bit of a curiosity.

It challenges the model of nerve cell functioning that was developed by Alan Hodgkin and Andrew Huxley, both of whom won the Nobel prize for their work.

Their discovery was that nerve cells can be understood as electrical circuits and that the transmission of nerve signals or action potentials can be described using a simple elegant mathematical formula.

This formula describes how nerve cells work remarkably well and is still the basis of much modern neuroscience.

So suggesting that the Hodgkin-Huxley model is wrong is likely to piss a lot of people off, and that's exactly what the Soliton model has done.

However, this new paper suggests it could explain how anaesthetics work, which is one of the mysteries of modern neuroscience.

It's a totally left-field idea, but if it works out, it would be a revolution in both neuroscience and medicine.

Quantum model of nerve pulse I: Soliton model of nerve pulse

In the first part of series I will briefly summarize soliton model of nerve pulse proposed by Danish researchers [1,2,3,4].

The temperature of the axon is slightly above the critical temperature T^c for the phase transition leading from crystal like state of the lipid layers to a liquid crystal state. Near criticality the elastic constants and heat capacity of the membrane vary strongly and have maxima at criticality so that also sound velocity varies strongly near criticality. Also the relaxation times are long. There is also dispersion present meaning that the frequency of sound wave depends nonlinearly on wave vector. Non-linearity and dispersion are prerequisites for the presence of solitons which by definition do not dissipate energy.
Variations of temperature, volume, area, and thickness and also other mechanical effects are known to accompany nerve pulse propagation. It is also known that the heat density and temperature of the cell membrane increases slightly first and is then reduced. This suggests adiabaticity in average sense. These findings motivate the assumption that nerve pulse actually corresponds to acoustic soliton [2,3].
Soliton model reproduces correctly the velocity of nerve pulse inside myelin sheaths but it is not clear to me how well the much lower conduction velocity in non-myelin sheathed regions is reproduced. It is not clear how the lower values of the conduction velocity and its proportionality to the axonal radius in non-myelinated regions can be understood. Intuitively it however seems clear that the lower velocity is due to the feedback from the interaction of ions with the region exterior to cell membrane. In the case of myelin sheaths the conduction of nerve pulse is usually believed to take place via saltation [6]: the depolarization induced at Ranvier node is believed to be enough to take the membrane potential below critical value in the next node so that nerve pulse hops between the nodes. Insulation would improve the insulation and make this process possible. The reversible heat transfer process is however known to be present also in the myelinated portions of axon so that there must be a pulse propagating also in these regions [3]. It is not clear how the myelin sheet can increase the velocity in the soliton model but the reduction of the feedback inducing friction suggests itself.
Soliton property predicts adiabaticity. Ordinary ionic currents however dissipate so that adiabaticity assumption is questionable in standard physics context. The model does not predict the growth of entropy followed by its reduction. This behavior is consistent with adiabaticity in a time resolution of order millisecond.
The estimate for the capacitor energy density during the nerve pulse is considerably smaller than the energy density is many times magnitude smaller than that of the acoustic wave. This might allow to demonstrate that Hodgkin-Huxley model is not a complete description of the situation.
Authors notice [2,3] that the shapes curves representing solitonic energy density and the capacitor energy density as a function of time are essentially identical. Same applies to the experimentally deduced heat change release curve and capacitor energy density for garfish axon. Also heat release and the deviation of the membrane potential from its resting value are in exact phase. These similarities could reflect a control signal responsible for the nerve pulse originating somewhere else, perhaps at microtubuli. This could explain why secondary nerve pulse is not generated immediately after the first one although the temperature is slightly lower after the pulse than before it. This could of course be also due to the exhaustion of the metabolic resources.

For background see that chapter Quantum Model of Nerve Pulse of "TGD and EEG".

References

[1] Soliton model.

[2] T. Heimburg and A. D. Jackson (2005), On soliton propagation in biomembranes and nerves, PNAS vol. 102, no. 28, p.9790-9795.

[3] T. Heimburg and A. D. Jackson (2005), On the action potential as a propagating density pulse and the role of anesthetics, arXiv : physics/0610117 [physics.bio-ph].

[4] K. Graesboll (2006), Function of Nerves-Action of Anesthetics, Gamma 143, An elementary Introduction.

[5] Physicists challenge notion of electric nerve impulses; say sound more likely.

[6] Saltation.

Quantum model of nerve pulse II: Basic inputs of TGD based model of nerve pulse

The model of nerve pulse whose inputs are summarized below can be motivated by the observed adiabaticity of the nerve pulse and by the strange findings about ionic currents associated with the cell membrane and by the model of Danish researchers for the nerve pulse [1,2,3,4]. The model involves also a fusion of various ideas of earlier models. In particular, Josephson currents and solitons are in a key role in the model but with the necessary flexibility brought in by the hierarchy of Planck constants.

The basic inputs of the model are following.

The presence of acoustic soliton or density pulse proposed by Danish researchers [3] looks plausible but a a more fundamental quantum control mechanism inducing the acoustic soliton cannot be excluded. Among other things this should explain why acoustic solitons propagate always in the same direction. In particular, one can consider a soliton like excitation (say breather for Sine-Gordon equation) associated with the electronic or ionic Josephson currents running along magnetic flux tubes. The strange effects associated with the ionic currents through the cell membrane suggest quite generally that at least weak ionic currents through normal cell membrane are non-dissipative quantal currents. The adiabaticity of the nerve pulse suggests that also strong ionic currents are quantal.
Strong ionic currents generating nerve pulse through axonal membrane are absent in the resting state. The naive explanation is simple: the life time of the magnetic flux tubes connecting the axonal interior to the exterior is short or the flux tubes are altogether absent. The observation that Josephson currents in constant voltage are automatically periodic suggests a less naive explanation allowing the flux tubes to be present all the time. The presence of ionic Josephson currents predicts a small amplitude oscillation of membrane potential for which 1 kHz synchronous oscillation is a natural identification. Josephson oscillation correspond naturally to propagating soliton sequences for Sine-Gordon equation [7]. The dynamics of the simplest modes is equivalent to the rotational motion of gravitational pendulum: the oscillation of membrane potential corresponds to the variation of dΦ/dt propto V. Note that if axon is above the melting temperature, the lipid layer is in gel phase and fluid motion is impossible. The surface density of lipids is dramatically reduced at criticality so that lipid layers behave like fluids [3]. This means that tqc is not possible by the braiding of lipids.
Nerve pulse is generated when the magnitude of the negative membrane potential is reduced below the critical value. Generation of the nerve pulse is like a kick to a rotating gravitational pendulum changing the sign of Ω= dΦ/dt so that rotational motion is transformed to oscillatory motion lasting for about the period of rotation. An opposite but slightly stronger kick must reduce the situation to the original one but with a slightly higher value of Ω. These kicks could correspond to voltage pulse between microtubules and inner lipid layer of cell membrane induced by the addition of small positive (negative) charge on lipid layer. This pulse would induce electronic DC Josephson current inducing the kick and thus reducing V. The exchange of scaled variants of W bosons (assignable to W MEs) could mediate the transfer of charge through the cell membrane and reduce the membrane potential below the critical value but one can consider also other mechanisms.
The conservative option would be that ordinary ionic currents take care of the rest and Hogkin-Huxley model applies. This was assumed in the earliest model in which soliton sequence for Josephson current was assumed to induce nerve pulse sequence: in the recent model this assumption does not make sense. The findings of Danish researchers do not however support the conservative option [3]. Nerve pulse could be due to dark ionic (possibly supra -) currents with large hbar with a low dissipation rate. Their flow would be made possible by the presence of magnetic flux tubes connecting cell interior and exterior.