WHO: Ahmed El Hadi, Postdoctoral Research Associate, Princeton Neuroscience Institute
WHEN: May 5th, 2015, 2:00-3:30pm
WHERE: AUB, West Hall, Auditorium A

For many decades, Action Potentials (APs) have been measured using electrophysiological methods and understood as electrical signals generated and propagating along the axonal membrane. In parallel, a large number of experimental studies have shown that the AP is accompanied by fast and temporary mechanical changes. These include changes in axonal radius and pressure, the release and subsequent absorption of a small amount of heat and shortening of the axon at its terminus when the AP arrives. Despite this wealth of experimental evidence, the physical basis for the mechanical and thermal signals that accompany the AP remains poorly understood.To our knowledge, there have been no attempts to quantitatively describe the mechanical component of the AP as an electrically driven phenomenon. We consider a minimal mechanical model of the axon as an elastic and dielectric tube filled and surrounded with viscous fluid. We show that as the AP passes, changes in charge separation across the dielectric membrane alter surface forces that act on the membrane’s geometry. As we show, these forces lead to co-propagating mechanical displacements which we call Action Waves (AWs). Our model predicts that the mechanical AW should propagate slightly ahead of the electrical AP.Thus, while it is possible that the AW is an epiphenomenon, it seems likely that biology would take advantage of this co-propagating information. Such a picture is broadly supported by experiments that see changes in electrical properties and even the triggering of APs on mechanical stimulation of single neurons. Membrane mechanical properties are known to influence some ion channels directly including the voltage gated sodium channels responsible for the AP. More likely relevant for the AP, a channel could directly sense displacements by connecting to a cytoskeletal element through a tether whose length is coupled to channel activity. Such a mechanism is thought to convert mechanical signals in the inner ear into electrical ones, where channels can sense displacements of 5 μm hair cells by as little as 0,3 nm, about as large as the radial displacements predicted by our model, and much smaller than the horizontal ones. Though this mechanism remains speculative even in the inner ear, Na channels do coordinate at nanometric scales with periodic actin rings and spectrin. Na channels are anchored to the cytoskeleton by ankyrin-G, which is homologous to the ankyrin repeats in specialized TRP channels widely believed to play the role of the mechanical to electrical transducer in the inner ear. This mechanical feedback on electrical properties might be seen to simply renormalize effective parameters of the cable theory, but the collective nature of mechanical modes leads to very different noise propagation perhaps allowing for more precise spike timing.Our model highlights the importance of incorporating mechanics into our understanding of nerve pulse propagation

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