By arguing against the theory you’re validating my title. Thanks for your expert opinion.
I’d like to point out before I address your critiques that this is not my theory and it is not going to upend decades of study if it is true. It simply explains phenomenon above and beyond what a purely electrical model of action potential signaling can.
So let’s go point by point:
Post action potential hyper-polarization — the dip in the tail of an action potential.
It seems to me that you bring this up because it is so well explained by potassium efflux. Are you suggesting that there is no role for ions to play in a model that explains the mechanical component of action potentials? Because you’ve misread this theory if you’re implying that ion channels, ion, and concentration/voltage gradients play no role at all. But beyond all that, the theory does address this question, to which it provides evidence about a subsequent cooling phase of the axon following a raise in local temperature during an action potential.
Neurotransmitter release when an action potential reaches the synapse.
Again, it seems like you’ve made a strawman out of the theory to argue that a mechanical model of action potential propagation would discount any role of ions in the process. This is just absurd and, dare I say it, intellectually dishonest. Calcium has a well-defined role in the fusion of vesicles to the plasma membrane and the progression of clathrin-mediated endocytosis. But, as I’ll discuss in response to your next question, there are questions about neurotransmitter release that cannot be explained by an electrical-only explanation of action potentials. I mean, how can you discount the role of mechanical forces in the process of vesicle fusion?!
The differential control of neurotransmitter and neuropeptide release from the same synapse by the frequency of action potentials.
I’m so glad you brought this up, because I discovered the Soliton Theory of Nerve Propagation while studying this exact question in graduate school. How is it that neurotransmitters and neuropeptides can be released from the same synapse?! And this same problem exists for the differential release of two different neurotransmitters from the same axon. Indeed, you’re arguing against your own claim here because the mechanical tension of the membrane at a synapse has been invoked to explain the clustering and fusion of vesicles for neurotransmitter release. A mechanical theory in particular is highly explanatory when it comes to the differential release of neuropeptides and neurotransmitters, because neuropeptide vesicles are much larger (~100nm) than neurotransmitter vesicles (~40nm). Although there are explanations that can be derived from a purely electrical-based model, a mechanical model can straightforwardly explain the difference through the degree of physical tension put on the membrane at higher frequencies of action potential — it’s a much more intuitive model for this very question. Do you have a preferred explanation for these phenomena?
The initiation of an action potential by the summation of EPSPs in the dendrites.
This is a good question to end on, because there are so many open questions about dendritic summation and back-propagation (as I touch on briefly in my article). Again, you seem to be mistaking a mechanical model for a complete eschewing of classical ion-based models — this just isn’t the case. But one thing that a purely electrical model does have trouble explaining is the role of back-propagation in dendrites and how this information can be integrated in spite of constant incoming signaling in a “forward” direction. Any thoughts on how this could occur?
Thanks for reading and I hope you’ll be willing to continue this discussion with an open mind. While it seems that you haven’t read the papers I’ve already linked to in the article, I’d love to share more resources about the topic if you’re actually interested in learning more.