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Hillel Ori

Publications and source records attributed to Hillel Ori.

3 recordsLinked to original sources

Spiking at the edge

Excitable media, ranging from bioelectric tissues and chemical oscillators to forest fires and competing populations, are nonlinear, spatially extended systems capable of spiking. Most investigations of excitable media consider situations where the amplifying and suppressing forces necessary for spiking coexist at every point in space. In this case, spiking requires a fine-tuned ratio between local amplification and suppression strengths. But, in Nature and engineered systems, these forces can be segregated in space, forming structures like interfaces and boundaries. Here, we show how boundaries can generate and protect spiking if the reacting components can spread out: even arbitrarily weak diffusion can cause spiking at the edge between two non-excitable media. This edge spiking is a robust phenomenon that can occur even if the ratio between amplification and suppression does not allow spiking when the two sides are homogeneously mixed. We analytically derive a spiking phase diagram that depends on two parameters: (i) the ratio between the system size and the characteristic diffusive length-scale, and (ii) the ratio between the amplification and suppression strengths. Our analysis explains recent experimental observations of action potentials at the interface between two non-excitable bioelectric tissues. Beyond electrophysiology, we highlight how edge spiking emerges in predator-prey dynamics and in oscillating chemical reactions. Our findings provide a theoretical blueprint for a class of interfacial excitations in reaction-diffusion systems, with potential implications for spatially controlled chemical reactions, nonlinear waveguides and neuromorphic computation, as well as spiking instabilities, such as cardiac arrhythmias, that naturally occur in heterogeneous biological media.

cond-mat.soft

Electric-induced reversal of morphogenesis in Hydra

Morphogenesis involves the dynamic interplay of biochemical, mechanical and electrical processes. Here we ask: to what extent can the course of morphogenesis be modulated and controlled by an external electric field? We show that above a critical amplitude, an external electric field can halt morphogenesis in Hydra regeneration. Moreover, above this critical amplitude, the electric field can even lead to reversal dynamics: a fully developed Hydra folds back into its incipient spheroid morphology. The potential to renew morphogenesis is re-exposed when the field is reduced back to amplitudes below criticality. These dynamics are accompanied by modulations of the Wnt3 activity, a central component of the head organizer in Hydra. Reversal of morphogenesis is shown to be triggered by enhanced epithelial electrical excitations, accompanied by intensified calcium activity, indicating that electrical processes play an instructive role to a level that can direct developmental trajectories. Reversal of morphogenesis by external fields, calls for extending its framework beyond programmatic, forward-driven, hierarchical processes.

physics.bio-ph

Cellular function given parametric variation: excitability in the Hodgkin-Huxley model

How is reliable physiological function maintained in cells despite considerable variability in the values of key parameters of multiple interacting processes that govern that function? Here we use the classic Hodgkin-Huxley formulation of the squid giant axon action potential to propose a possible approach to this problem. Although the full Hodgkin-Huxley model is very sensitive to fluctuations that independently occur in its many parameters, the outcome is in fact determined by simple combinations of these parameters along two physiological dimensions: Structural and Kinetic (denoted $S$ and $K$). Structural parameters describe the properties of the cell, including its capacitance and the densities of its ion channels. Kinetic parameters are those that describe the opening and closing of the voltage-dependent conductances. The impacts of parametric fluctuations on the dynamics of the system, seemingly complex in the high dimensional representation of the Hodgkin-Huxley model, are tractable when examined within the $S-K$ plane. We demonstrate that slow inactivation, a ubiquitous activity-dependent feature of ionic channels, is a powerful local homeostatic control mechanism that stabilizes excitability amid changes in structural and kinetic parameters.

q-bio.NC