The Dominant Model in Neuroscience is Wrong
Minute electrical impulses tend to be easier to measure with instruments than minute mechanical impulses. The nerve cell (or neuron) has both, but due to the former being easier to measure, and perhaps for many other unknown reasons, the theory that came to dominate was the one we are all familiar with today — that the neuron communicates a signal to another neuron electrically. This is called the Hodgkin-Huxley model after the two men measured a voltage spike across the membrane of a firing neuron in 1952.
This widely believed theory is wrong. The way in which many believe anesthetics works is also wrong.
Failure of the Hodgkin-Huxley Model
The way in which anesthetics appear to work is inconsistent with the model.
The nerve cell allows sodium or potassium ions to flow in and out of the membrane through valves (ion channels). According to the Hodgkin-Huxley model, anesthetics work by blocking these ion channels and thus blocking the electrical signal of the cell; but given the variety of molecular forms of anesthetics, there is no explanation for how they can all block these channels which take specific shapes to allow sodium and potassium ions to flow. Furthermore, dozens of anesthetics were placed in water and olive oil (Ernest Overton, 1901) and the more potent the anesthetic (in animals), the more it moved into the oil. Coincidentally, olive oil and the fatty acids within nerve cell membranes are very similar. This means that it is far more likely that anesthetics work by being absorbed into the membrane rather than blocking ion channels of the membrane. As we will soon see, the anesthetic works by raising the phase transition of the fatty acid (making it harder for it to go from liquid to solid state).
Nerve fiber signals travel too slow to be electrical signals.
Nerve fibers carry signals across the body at roughly 30m/s, or 70mph. Electrical signals tend to be orders of magnitude faster than this. Thus, the signal is either a complicated chemical process that is far slower than other electrical signals, or the signal is not electrical but something else.
The visual changes of the nerve cell are not explained by the model.
From the 1940s, it has been observed that neurons become opaque when they fire and return to their original translucent state. The current model does not explain this phenomena.
The heat transfer during the firing process is inconsistent with the model.
In the late 1960s and onward, heat transfer was observed as neurons fired, but the process was peculiar to researchers. The neural cell released heat when firing (which is consistent with electrical pulsing), but reabsorbed the heat almost instantly right after firing (which is not explained via electrical pulsing). That is, the heat from the firing was not dissipating but was being reabsorbed into the cell, returning it to its original state.
The physical changes of the cell is not explained by the model.
Along the lines of the heat release-absorption, at the same time, researchers found that the molecules in the membrane were physically rearranging themselves as the heat spiked and then rearranging themselves back after the spike.
The physical movement of the cell is not explained by the model.
Lastly, the nerve cell physically contracts during the firing process, which is also not explained in the current theory.
There is of course, a much better explanation of these phenomena, but it is not the Hodgkin-Huxley model of electrical signals.
A New Theory
The nerve cell mechanically contracts and expands back in a shock wave.
In 1979, Ichiji Tasaki placed a speck of platinum on a neural bundle, shined a laser on it, and measured the deflection as it fired. The firing process of a signal was mechanical! Since then, with finer microscopes and lasers, the contraction or mechanical wave across firing neurons has been observed repeatedly.
The nerve cell membrane undergoes a phase change.
Thomas Heimburg compressed artificial cell membranes in the 1990s, revealing that the fatty acids within are fluids but exist close to a phase transition. If the membrane is squeezed, the fluid turns into a near-crystal. That is, the randomly-oriented fluid becomes something in between a fluid and a solid when compressed. Phase transitions, by the way, explain the heat dilemma mentioned above. As a liquid becomes a solid or a gas becomes a liquid, heat is released. In the opposite direction, heat is absorbed. The fatty acids become crystal-like and releases heat because they are losing energy (liquids have more molecular energy than solids). The fatty acids then revert back to a fluid as the mechanical pulse passes and reabsorb the lost heat. This shock wave is what Tasaki observed with his speck of platinum and laser deflection.
The membrane’s phase change can be caused by voltage or pressure.
On the matter of the voltage pulse observed, Heimburg could use voltage to put the fatty acids into the liquid-crystal state. This process is the converting of electrical forces into mechanical forces, and vice versa. The class of materials known for such processes are referred to as piezoelectric materials, and it is becoming quite clear to some that the membrane of neural cells contain such materials.
Laboratory shock wave speeds match real nerve cell signal speeds.
The shock waves produced in artificial membranes travel at a similar speed as those observed in real neural cells (Matthias Schneider, 2009), and those shock waves were both mechanical and electrical (Schneider, 2012).
Anesthetics are absorbed into the membrane rather than block ion channels.
If the Hodgkin-Huxley model is true, then anesthetics must somehow block the electrical signal that the neuron fires, but it has been observed (1942) that tadpoles under anesthetics can regain movement under higher pressure and higher voltage. If higher pressure negates the effects of anesthetics, then it is likely that the anesthetic is being absorbed (rather than blocking ion channels, or “blocking the electrical signal”) into the fatty acids. This lowers the required temperature and raises the require pressure required for the phase transition to occur, by sort of making the fatty acids more relaxed.
The purpose of the ion channel is to pressurize the membrane
The ion channels let ions flow in and out, creating a voltage across the membrane (pressure!). This force compresses the membrane, putting it closer to the phase transition state. If healthy with enough ions present, the channels will create just enough pressure across the membrane that a small stimuli will trigger the membrane to contract and undergo phase transition.