Simulation of Oculomotor Post-Inhibitory Rebound Burst Firing using a Hodgkin-Huxley Model of a Neuron.

A number of theories have been reported on post saccade phenomenon describing dynamic overshoot, glissadic overshoot and undershoot, and undershoot, all naturally and frequency occurring saccadic eye movements. Electrophysiological evidence for post-inhibitory rebound burst firing activity during saccadic eye movements is prevalent in the literature. However, the cause for the phenomenon is not known. Marked inhibition of neurons within the Paramedian Pontine Reticular Formation often results in post-inhibitory rebound burst firing activity at the beginning and end of a saccade. In this paper, post-inhibitory rebound burst firing activity after marked hyperpolarization is postulated to occur in the Paramedian Pontine Reticular Formation due to a low membrane threshold voltage. With this biophysical property, a single neuron is capable of firing at high rates automatically and without stimulation when released from inhibition. Simulations using the Hodgkin-Huxley model of a neuron demonstrate that a single neuron is capable of firing at high rates automatically without stimulation when released from inhibition.