The Thermodynamic Model to Study the Slow Afterhyperpolarization in a Single Neuron at Different ATP Levels

TL;DR

This paper presents a thermodynamic model that explains how ATP levels influence the slow afterhyperpolarization in neurons, highlighting the roles of NKA and K(Ca) channels in energy-dependent neural behavior.

Contribution

The study introduces a novel thermodynamic model linking ATP hydrolysis to sAHP modulation, providing quantitative insights into energy-dependent neuronal processes.

Findings

sAHP amplitude depends on intracellular ATP concentration

Trade-off between NKA and K(Ca) in energy modulation of sAHP

Altered sAHP behavior under low ATP conditions predicted

Abstract

The neuron consumes energy from ATP hydrolysis to maintain a far-from-equilibrium steady state inside the cell, thus all physiological functions inside the cell are modulated by thermodynamics. The neurons that manage information encoding, transferring, and processing with high energy consumption, displaying a phenomenon called slow afterhyperpolarization after burst firing, whose properties are affected by the energy conditions. Here we constructed a thermodynamical model to quantitatively describe the sAHP process generated by $Na^+-K^+$ ATPases(NKA) and the Calcium-activated potassium(K(Ca)) channels. The model simulates how the amplitude of sAHP is effected by the intracellular ATP concentration and ATP hydrolysis free energy $\Delta$ G. The results show a trade-off between NKA and the K(Ca)'s modulation on the sAHP's energy dependence, and also predict an alteration of sAHP's behavior under insufficient ATP supply if the proportion of NKA and K(Ca)'s expression quantities is changed. The research provides insights in understanding the maintenance of neural homeostasis and support furthur researches on metabolism-related and neurodegenerative diseases.