Energy consumption of spontaneous up–down oscillations modulated by ion channel inactivation

In clinical practice, sodium and potassium channels are considered targets of action for a variety of drugs (e.g., propofol, curcumin, etc.). Most of the studies are based on physiological experiments in which researchers have investigated the effects of ion channel residues on the conductance and homeostatic inactivation processes of ion channels by means of gene targeting mutation techniques. However, few researchers investigate the effects of voltage-gated ion channel properties on neural network behavior based on kinetic models. In this paper, we systematically vary the conductivity per unit area or the inactivation time constant to model the effects of drugs on ion channels. Numerical results show that, persistent sodium dynamics affect the firing rate and energy consumption of the neural network as much as fast sodium dynamics does. And the high synchronization rate of the neural network significantly enhances the firing rate of the network. In addition, we find that the network’s excitability is significantly increased by enhancing potassium channel inactivation, whereas enhanced inactivation of sodium channels can rapidly inhibit network excitability. These simulations are in general consistent with the experimental results. Our research provides a perspective on understanding the process of drug regulation of ion channels from a kinetic perspective.