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Ben Machta

Princeton University

Title: Mechanical surface waves accompany action potential propagation

Abstract: Diverse studies have shown that a mechanical displacement of the axonal membrane accompanies the electrical pulse that defines the action potential (AP). I will present a model for these mechanical displacements as arising from the driving of surface wave modes in which potential energy is stored in elastic properties of the neuronal membrane and cytoskeleton while kinetic energy is carried by the axoplasmic fluid. In our model, these surface waves are driven by the traveling wave of electrical depolarization characterizing the AP, altering compressive electrostatic forces across the membrane. This driving leads to co-propagating mechanical displacements, which we term Action Waves (AWs). Our model allows us to estimate the shape of the AW that accompanies any travelling wave of voltage, making predictions for lateral and longitudinal displacements and thermal signatures that are in agreement with results from several experimental systems. Our model can serve as a framework for understanding the physical origins and possible functional roles of these AWs. (El Hady and Machta, Nat Comm 6, 6697 (2015)). I will also report on our recent inquiry into the role of membrane criticality in mediating anesthesia. We have previously shown that n-alcohol anesthetics take cell derived plasma membrane vesicles away from their naturally tuned liquid-liquid miscibility critical point by lowering Tc in a manner that is quantitatively predicted by their potency (Gray et. al., Biophys J. 105 12). Here I will show that treatments that reverse anesthesia reverse effects on membrane criticality as well, actually raising critical temperatures (Arxiv 1604.00412). These results suggest that anesthetics may exert their effects on ion channels indirectly, by interfering with native regulation of function by membrane domains.

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