Controversial New Idea: Nerves Transmit Sound, Not Electricity
By Robert Roy Britt
LiveScience Managing Editor
Nerves transmit sound waves through your body, not electrical pulses, according to a controversial new study that tries to explain the longstanding mystery of how anesthetics work.
Textbooks say nerves use electrical impulses to transmit signals from the brain to the point of action, be it to wag a finger or blink an eye.
"But for us as physicists, this cannot be the explanation," says Thomas Heimburg, a Copenhagen University researcher whose expertise is in the intersection of biology and physics. "The physical laws of thermodynamics tell us that electrical impulses must produce heat as they travel along the nerve, but experiments find that no such heat is produced."
The textbooks are not likely to be rewritten anytime soon, however.
Roderic Eckenhoff, a researcher in the Department of Anesthesiology and Critical Care at the University of Pennsylvania School of Medicine, called the sound pulse idea interesting. "But an enormous burden of proof exists and they have a very long way to go to beat electricity," he said.
The olive oil clue
Nerves are wrapped in a membrane of lipids and proteins. Biology textbooks say a pulse is sent from one end of the nerve to the other with the help of electrically charged salts that pass through ion channels in the membrane. But the lack of heat generation contradicts the molecular biological theory of an electrical impulse produced by chemical processes, says Heimburg, who co-authored the new study with Copenhagen University theoretical physicist Andrew Jackson.
Instead, nerve pulses can be explained much more simply as a mechanical pulse of sound, Heimburg and Jackson argue. Their idea will be published in the Biophysical Journal.
Normally, sound propagates as a wave that spreads out and becomes weaker and weaker. But in certain conditions, sound can be made to travel without spreading and therefore it retains its intensity.
The lipids in a nerve membrane are similar to olive oil, the scientists explain. And the membrane has a freezing point that is precisely suited to the propagation of these concentrated sound pulses [graphic].
Eckenhoff is not convinced, however.
"It is difficult to explain away an enormous number of real electrical recordings in the cell, tissue and whole animal as being some kind of artifact," Eckenhoff told LiveScience. "And I cannot easily discern how the sound might be generated."
Explaining anesthesia
The idea from Heimburg and Jackson, if it were proven true, could have implication for anesthetics, another mysterious process.
Oddly, scientists don't understand exactly what happens when a patient is anesthetized. While the goal of an anesthetic is to prevent the brain from feeling pain, the drugs can affect a patient's heart rate and breathing. So a better understanding of how it all works would allow development of better drugs.
Researchers do know that the proper doses of ether, laughing gas, chloroform and other anesthetics are all based on their solubility in olive oil. But how the nerves are turned off is a mystery.
Heimburg and Jackson offer an explanation.
If a nerve is to be able to transport sound pulses, they say, then the melting point of its membrane must be close to body temperature. Anesthetics change the melting point so that sound pulses can't propagate, they conclude. Nerves are put on stand-by and a patient doesn't feel the knife slicing into his body.
While Eckenhoff acknowledges there is much to learn, he expects the precise effects of anesthesia will ultimately be explained by an integration of current theories rather than by employing the new idea of sound pulses.
Full Version: Nerves Transmit Sound, Not Electricity
from Wikipedia:
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.
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.
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.
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.
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.
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.
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.
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.
this Thomas Heimburg sounds like a quack
This is Thomas Heimburg's main paper dealing with this Soliton theory:
http://www.pnas.org/cgi/content/abstract/102/28/9790
On soliton propagation in biomembranes and nerves
Thomas Heimburg *, and Andrew D. Jackson
The Niels Bohr Institute, University of Copenhagen, 17 Blegdamsvej, 2100 Copenhagen Ø, Denmark
Communicated by Gordon A. Baym, University of Illinois at Urbana–Champaign, Urbana, IL, May 9, 2005 (received for review February 14, 2005)
The lipids of biological membranes and intact biomembranes display chain melting transitions close to temperatures of physiological interest. During this transition the heat capacity, volume and area compressibilities, and relaxation times all reach maxima. Compressibilities are thus nonlinear functions of temperature and pressure in the vicinity of the melting transition, and we show that this feature leads to the possibility of soliton propagation in such membranes. In particular, if the membrane state is above the melting transition solitons will involve changes in lipid state. We discuss solitons in the context of several striking properties of nerve membranes under the influence of the action potential, including mechanical dislocations and temperature changes.
and here's the conclusion from the PNAS paper:
It is clear that the Hodgkin–Huxley model fails to explain a number of features of the propagating nerve pulse, including the reversible release and reabsorption of heat and the accompanying mechanical, fluorescence, and turbidity changes. The most striking feature of the isothermal and isentropic compression modulus is its significant undershoot and striking recovery. These features lead generically to the conclusions (i) that there is a minimum velocity of a soliton and (ii) that the soliton profiles are remarkably stable as a function of the soliton velocity. There is a maximum amplitude and a minimum velocity of the solitons that is close to the propagation velocity in myelinated nerves. In addition, solitons propagate without distortion of their form. It would be surprising if nature did not exploit these features.
It is clear that the Hodgkin–Huxley model fails to explain a number of features of the propagating nerve pulse, including the reversible release and reabsorption of heat and the accompanying mechanical, fluorescence, and turbidity changes. The most striking feature of the isothermal and isentropic compression modulus is its significant undershoot and striking recovery. These features lead generically to the conclusions (i) that there is a minimum velocity of a soliton and (ii) that the soliton profiles are remarkably stable as a function of the soliton velocity. There is a maximum amplitude and a minimum velocity of the solitons that is close to the propagation velocity in myelinated nerves. In addition, solitons propagate without distortion of their form. It would be surprising if nature did not exploit these features.
I'm shocked and amazed that they don't fully understand the mechanism behind an anesthetic. I will be slightly more worried the next time myself or a friend goes into surgery.
I think that the sound theory is "sound" lol. There was a recent breakthrough that allows streams of sound to be projected silently and separately until it hits a surface. At this point it recombines into an audible sound. The inventor had lots of fun scaring kids at halloween. No idea what the technology was called though.
I think that the sound theory is "sound" lol. There was a recent breakthrough that allows streams of sound to be projected silently and separately until it hits a surface. At this point it recombines into an audible sound. The inventor had lots of fun scaring kids at halloween. No idea what the technology was called though.
Wonder what those foetuses reckon to all that (ultra)sound?
I'm confused. In the first post you get ""The physical laws of thermodynamics tell us that electrical impulses must produce heat as they travel along the nerve, but experiments find that no such heat is produced."
and then in the second post from Wikipedia (not to be trusted) you get: "It has been known for several decades that an action potential traveling along a neuron results in a slight increase in temperature..."
Thomas Heimburg does indeed sound like a quack!
and then in the second post from Wikipedia (not to be trusted) you get: "It has been known for several decades that an action potential traveling along a neuron results in a slight increase in temperature..."
Thomas Heimburg does indeed sound like a quack!
Heat production known from long back, e.g.:
The origin of the initial heat associated with a single impulse in mammalian non-myelinated nerve fibres
J. V. Howarth, R. D. Keynes, and J. M. Ritchie
J Physiol 194(3) Feb 1968
Abstract
1. A study has been made of the temperature changes associated with the passage of a single impulse in rabbit desheated vagus nerves.
2. The initial changes consist of an evolution of positive heat followed by a reabsorption of most of it; i.e. there is a phase of positive and a phase of negative heat production.
3. The size of the positive heat, its time of onset, and the time of onset of the negative heat have been measured by an analogue method of analysis. In addition, these parameters, together with the size of the negative heat and the duration of both phases of initial heat, have been studied with the aid of a computer, and also by conventional heat block analysis.
4. At about 5° C the measured positive heat is 7·2 ?cal/g. impulse. It starts as soon as the compound action potential reaches the thermopile and lasts for about 107 msec.
5. This positive heat decreases with increasing temperature, the ratio of heat at 4° C to that at 14° C being 1·86.
6. The measured negative heat at about 5° C is 4·9 ?cal/g. impulse. It starts 102 msec after the onset of positive heat, and lasts for about 240 msec.
7. When the sodium of Locke solution is replaced by lithium the positive heat is reduced by 19%, but the negative heat is increased by 22%.
8. In potassium-free solutions the positive heat is hardly affected (increase of 5%), but the negative heat is more than doubled. As a result the nerve may become briefly colder than its initial temperature by about 2 ?° C.
9. The effect of sodium-deficient solutions on the positive heat is somewhat variable, but the negative heat is consistently diminished.
10. Replacement of the chloride of Locke solution by sulphate or nitrate has little effect on the positive heat. The negative heat is reduced in size by 26% and in duration by 22%.
11. Replacement of most of the sodium of Locke solution by barium reduces or abolishes the negative heat, and increases the measured size of the positive heat nearly threefold.
12. Veratrine (10-5 g/ml.) produces a nearly tenfold increase in the net positive heat.
13. Ouabain (1 mM) and antimycin A (1 ?g/ml.) applied for 30-60 min have little effect on the initial heat production.
14. Over the temperature range 5-15° C, and for the ionic solution changes described above, there is close agreement in timing between the positive heat and the rising phase of the action potential, and between the negative heat and the falling phase.
15. Because of the inevitable temporal dispersion of the action potential over the face of the thermopile, the observed temperature changes are smaller than those which occur at a single point in the nerve close to a stimulating electrode. The corrected value of the positive heat at 5° C is 24·5 ?cal/g. impulse, while that of the negative heat is 22·2 ?cal/g. impulse.
16. The heats of mixing of the ions in solution that interchange during the action potential are much too small to account for the observed initial heats, but an exchange of ions associated with fixed charges might make a significant contribution to the heats.
17. The condenser theory, according to which the positive heat represents the dissipation of electrical energy stored in the membrane capacity, while the negative heat results from the recharging of the capacity, appears unable to account for more than half of the observed temperature changes.
18. It seems probable that the greater part of the initial heat results from changes in the entropy of the nerve membrane when it is depolarized and repolarized.
The origin of the initial heat associated with a single impulse in mammalian non-myelinated nerve fibres
J. V. Howarth, R. D. Keynes, and J. M. Ritchie
J Physiol 194(3) Feb 1968
Abstract
1. A study has been made of the temperature changes associated with the passage of a single impulse in rabbit desheated vagus nerves.
2. The initial changes consist of an evolution of positive heat followed by a reabsorption of most of it; i.e. there is a phase of positive and a phase of negative heat production.
3. The size of the positive heat, its time of onset, and the time of onset of the negative heat have been measured by an analogue method of analysis. In addition, these parameters, together with the size of the negative heat and the duration of both phases of initial heat, have been studied with the aid of a computer, and also by conventional heat block analysis.
4. At about 5° C the measured positive heat is 7·2 ?cal/g. impulse. It starts as soon as the compound action potential reaches the thermopile and lasts for about 107 msec.
5. This positive heat decreases with increasing temperature, the ratio of heat at 4° C to that at 14° C being 1·86.
6. The measured negative heat at about 5° C is 4·9 ?cal/g. impulse. It starts 102 msec after the onset of positive heat, and lasts for about 240 msec.
7. When the sodium of Locke solution is replaced by lithium the positive heat is reduced by 19%, but the negative heat is increased by 22%.
8. In potassium-free solutions the positive heat is hardly affected (increase of 5%), but the negative heat is more than doubled. As a result the nerve may become briefly colder than its initial temperature by about 2 ?° C.
9. The effect of sodium-deficient solutions on the positive heat is somewhat variable, but the negative heat is consistently diminished.
10. Replacement of the chloride of Locke solution by sulphate or nitrate has little effect on the positive heat. The negative heat is reduced in size by 26% and in duration by 22%.
11. Replacement of most of the sodium of Locke solution by barium reduces or abolishes the negative heat, and increases the measured size of the positive heat nearly threefold.
12. Veratrine (10-5 g/ml.) produces a nearly tenfold increase in the net positive heat.
13. Ouabain (1 mM) and antimycin A (1 ?g/ml.) applied for 30-60 min have little effect on the initial heat production.
14. Over the temperature range 5-15° C, and for the ionic solution changes described above, there is close agreement in timing between the positive heat and the rising phase of the action potential, and between the negative heat and the falling phase.
15. Because of the inevitable temporal dispersion of the action potential over the face of the thermopile, the observed temperature changes are smaller than those which occur at a single point in the nerve close to a stimulating electrode. The corrected value of the positive heat at 5° C is 24·5 ?cal/g. impulse, while that of the negative heat is 22·2 ?cal/g. impulse.
16. The heats of mixing of the ions in solution that interchange during the action potential are much too small to account for the observed initial heats, but an exchange of ions associated with fixed charges might make a significant contribution to the heats.
17. The condenser theory, according to which the positive heat represents the dissipation of electrical energy stored in the membrane capacity, while the negative heat results from the recharging of the capacity, appears unable to account for more than half of the observed temperature changes.
18. It seems probable that the greater part of the initial heat results from changes in the entropy of the nerve membrane when it is depolarized and repolarized.
I would just like to say that Heimburg and Jackson paper in PNAS 2005, 102:9790 does not challenge the Hodgkn and Huxley theory of signal propagation in the nerve, but points out a number of features of signal propagation not contained within the Hodgkin and Huxley theory. Those features may have biological applications. In authors' own words: "it would be surprising if nature did not exploit these features". Most of the scientific theories available to us (including the action of anesthetics) are not complete but are meant to describe reality in the best way we've so far managed to understand it.
QUOTE(utnap @ Mar 21, 2007, 09:21 PM) 
I would just like to say that Heimburg and Jackson paper in PNAS 2005, 102:9790 does not challenge the Hodgkn and Huxley theory of signal propagation in the nerve, but points out a number of features of signal propagation not contained within the Hodgkin and Huxley theory. Those features may have biological applications. In authors' own words: "it would be surprising if nature did not exploit these features". Most of the scientific theories available to us (including the action of anesthetics) are not complete but are meant to describe reality in the best way we've so far managed to understand it.
Yer but, no but, yer but the statement from J. V. Howarth, R. D. Keynes, and J. M. Ritchie in 1968:"The physical laws of thermodynamics tell us that electrical impulses must produce heat as they travel along the nerve, but experiments find that no such heat is produced."
shows that Heimburg has a very poor knowledge of the basic literature (found in 30 seconds on the internet) that does not inspire confidence in this worker.
Nicely done, Hey Hey. If you could shoot down a quack theory every day, we'd all be better off.
I think heat is produced, it is just very small. If you look at the sources for wikipedia, it gives this:
Ritchie JM, Keynes RD (1985). The production and absorption of heat associated with electrical activity in nerve and electric organ. Q Rev Biophys. 1985 Nov;18(4):451-76.
Which is the same author, Ritchie, as the 1968 article.
I don't have access to pubmed right now, but according to wikipedia this article shows that "An action potential traveling along a neuron results in a slight increase in temperature followed by a decrease in temperature". It is probably a small temperature change that was hard to detect with 1968 technology.
Ritchie JM, Keynes RD (1985). The production and absorption of heat associated with electrical activity in nerve and electric organ. Q Rev Biophys. 1985 Nov;18(4):451-76.
Which is the same author, Ritchie, as the 1968 article.
I don't have access to pubmed right now, but according to wikipedia this article shows that "An action potential traveling along a neuron results in a slight increase in temperature followed by a decrease in temperature". It is probably a small temperature change that was hard to detect with 1968 technology.
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