No one quite knows how nerve cells learn stuff. It is incorrectly thought that you can not get new nerves in the brain, nor that you can get brain cells to grow out further, but people have made new nerve cells, and when I was a professor at Michigan State, a Physiology colleague and I got brain and sensory nerves to grow out axons by pulling on them without the use of drugs.
I had just moved to Michigan State as a fresh PhD (Princeton) as an assistant professor of chemical engineering. Steve Heidemann was a few years ahead of me, a Physiology professor PhD from Princeton. We were both new Yorkers. He had been studying nerve structure, and wondered about how the growth cone makes nerves grow out axons (the axon is the long, stringy part of the nerve). A thought was that nerves were structured as Snelson-Fuller tensegrity structures, but it was not obvious how that would relate to growth or anything else. A Snelson-Fuller structure is shown below the structure stands erect not by compression, as in a pyramid or igloo, but rather because tension in the wires helps lift the metal pipes, and puts them in compression. The nerve cell, shown further below is similar with actin-protein as the outer, tensed skin, and a microtubule-protein core as the compress pipes.
Biothermodynamics was pretty basic 30 years ago (It still is today), and it was incorrectly thought that objects were more stable when put in compression. It didn’t take too much thermodynamics on my part to show otherwise, and so I started a part-time career in cell physiology. Consider first how mechanical force should affect the Gibbs free energy, G, of assembled microtubules. For any process at constant temperature and pressure, ∆G = work. If force is applied we expect some elastic work will be put into the assembled Mts in an amount ∫f dz, where f is the force at every compression, and ∫dz is the integral of the distance traveled. Assuming a small force, or a constant spring, f = kz with k as the spring constant. Integrating the above, ∆G = ∫kz dz = kz2; ∆G is always positive whether z is positive or negative, that is the microtubule is most stable with no force, and is made less stable by any force, tension or compression.
Assuming that microtubules in the nerve- axon are generally in compression as in the Snelson-Fuller structure, then pulling on the axon could potentially reduce the compression. Normally, this is done by a growth cone, we posited, but we could also do it by pulling. In either case, a decrease in the compression of the assembled microtubules should favor microtubule assembly.
To calculate the rates, I used absolute rate theory, something I’d learned from Dr. Mortimer Kostin, a most-excellent thermodynamics professor. I assumed that the free energy of the monomer was unaffected by force, and that the microtubules were in pseudo- equilibrium with the monomer. Growth rates were predicted to be proportional to the decrease in G, and the prediction matched experimental data.
Our few efforts to cure nerve disease by pulling did not produce immediate results; it turns out to by hard to pull on nerves in the body. Still, we gained some publicity, and a variety of people seem to have found scientific and/or philosophical inspiration in this sort of tensegrity model for nerve growth. I particularly like this review article by Don Ingber in Scientific American. A little more out there is this view of consciousness life and the fate of the universe (where I got the cell picture). In general, tensegrity structures are more tough and flexible than normal construction. A tensegrity structure will bend easily, but rarely break. It seems likely that your body is held together this way, and because of this you can carry heavy things, and still move with flexibility. It also seems likely that bones are structured this way; as with nerves; they are reasonably flexible, and can be made to grow by pulling.
Now that I think about it, we should have done more theoretical or experimental work in this direction. I imagine that pulling on the nerve also affects the stability of the actin network by affecting the chain configuration entropy. This might slow actin assembly, or perhaps not. It might have been worthwhile to look at new ways to pull, or at bone growth. In our in-vivo work we used an external magnetic field to pull. We might have looked at NASA funding too, since it’s been observed that astronauts grow in outer space by a solid inch or two, and their bodies deteriorate. Presumably, the lack of gravity causes the calcite in the bones to grow, making a person less of a tensegrity structure. The muscle must grow too, just to keep up, but I don’t have a theory for muscle.
Robert Buxbaum, February 2, 2014. Vaguely related to this, I’ve written about architecture, art, and mechanical design.