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Lyoubi-Idrissi, A.

Publications and source records attributed to Lyoubi-Idrissi, A..

2 recordsLinked to original sources

Resolving the Brain Energy Paradox: The Neuron as a Coupled Thermodynamic System

Traditional models of neural excitability, such as the Hodgkin-Huxley framework, treat the action potential as a purely electrical phenomenon. While its thermodynamic footprint--including heat and entropy generation--is experimentally known, it is typically regarded as a passive consequence of signal propagation. This work explores the hypothesis that this thermodynamic output is not passive, but instead plays an active role in modulating neural function. To investigate this, we developed a novel, fully coupled electro-thermo-entropic model where the entropy generated by an action potential directly feeds back to influence the kinetics of ion channels. Our simulations demonstrate a profound consequence of this coupling: the action potential undergoes progressive self-amplification, driven by a massive acceleration of its underlying kinetics. As the signal propagates, its peak amplitude grows significantly while its temporal duration remains remarkably stable. Furthermore, a statistical analysis reveals that this mechanism relies on the system operating as a robust thermodynamic switch, transitioning between a low-entropy quiescent state and a high-dissipation active state. Finally, we show that achieving this high-performance, amplifying state requires a disproportionately high energetic cost, a finding we term the Intelligence Premium. These results suggest that the action potential is a coupled electro-thermodynamic process that actively enhances its own strength and reliability. Our model offers a candidate mechanism for how waste energy is repurposed into a functional signal, providing a physical explanation for the brains high energy consumption and opening new perspectives on the link between thermodynamics and computation.

neuroscience↗

Non-equilibrium Thermodynamics Modulate TRPV1 Channel Activation via Tissue Entropy Production

Inflammatory processes involve complex interactions between molecular signaling and biophysical mechanisms, yet the thermodynamic consequences of such processes remain underexplored. Here, we present a theoretical multiscale model that demonstrates how elevated entropy production in inflamed tissue environments modulates the activation threshold of TRPV1 thermosensitive ion channels. Our framework integrates axonal electrophysiology based on the Hodgkin-Huxley formalism, thermodynamic heat transfer with explicit entropy generation, and a dynamic model of TRPV1 channel gating. Simulations reveal that increased entropy production leads to a downward shift in the activation temperature of TRPV1 channels, driven by cumulative non-equilibrium thermodynamic effects. This result provides a mechanistic explanation for the enhanced excitability of sensory axons in inflamed tissue and highlights entropy production as a fundamental physical variable influencing ion channel behavior. The study contributes a novel perspective on the coupling between thermodynamics and sensory transduction at the cellular level.

neuroscience↗