Computational modeling of bursting pacemaker neurons in the pre-Bötzinger complex

Abstract

Bursting pacemaker neurons in the pre-Bötzinger complex (pBC) were modeled in the Hodgkin–Huxley style. The single neuron model included rapidly inactivating sodium, persistent sodium, and delayed-rectifier potassium currents. The kinetics of the rapidly inactivating and persistent sodium channels was modeled using experimental data obtained from whole-cell patch clamp recordings from pBC neurons in vitro. Our computational study focused on the conditions that could provide the generation of endogenous bursting activity in single pacemaker neurons and neural populations and on the specific roles of voltage-gated potassium and persistent sodium currents in triggering or suppression of endogenous population oscillations in the pBC.