Medical How Anesthesia Works on the Brain

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A team of researchers from a Duke University found that several different general anesthesia drugs knock out the patient by hijacking the neural circuitry that the person falls asleep.

In a new study published online in Neuron, scientists believe they have discovered the part of the answer. A team of researchers from a Duke University found that several different general anesthesia drugs knock out the patient by hijacking the neural circuitry that the person falls asleep.

Does this disprove the soliton model of neuroscience? specifically "Application to anesthesia"

"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.[25] 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."


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I find it interesting that anesthetics could be affecting a brain center that controls sleep.
When I was in grad school, the story on anesthetics was that they probably got into membranes and changed their properties, thus probably affecting the membrane proteins that are commonly thought to underlie much of neuronal function.

The soliton idea I had not heard of before, but the wikipedia article points out some problems with it:
However these mechanical waves differ in fundamental ways from the properties described by the Hodgkin-Huxley Model in that they do not exhibit the very specific ionic selectivity, voltage sensitivity, time-course, or sensitivity to toxins that are integral to the Hodgkin-Huxley model.
Such thermal fluctuations cannot explain the specific ionic selectivity or the specific time-course of the response to voltage changes.
Those and the section on Differences between model predictions and experimental observation, leave me somewhat skeptical about it.
In addition, it sounds like the soliton explanation would only be used for action potentials, but not for other kinds of neural activity (which would presumably be underlain by more usual molecular-electrochemical explanations).
If so, at what point in the world of different neuronal electrical activity would the preferred explanation transition from the traditional molecular-electrochemical eplanation to solitons?
What about neural activity which is kind of between active (action potential) and passive spread?

I suppose that one could argue that both explanations could be relevant to different degrees in different situations.
In that case, the new anesthesia findings would, perhaps, not disprove the soliton hypothesis, but certainly don't lend it any support.
This is just anecdotal: my mother's father never needed anesthesia at the dentist's. He could fall asleep in the chair, and be submitted to drilling, etc.., and all the dentist had to do to wake him up after the procedure was to shake him by the shoulder a little while telling him it was time to wake up.

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