OBJECTIVEThe optic nerve is a key component regarding research on visual prosthesis. Previous pharmacological and electrical studies has pinned down the main features of the mechanisms underlying the nerve impulse in the rat optic nerve, and this work proposed a mathematical model to simulate these phenomena.

METHODSThe main active nodal channels: fast Na+, persistent Na+, slow K+ and a fast repolarizing K+ (A-current) were added on a double layer representation of the axon. A simplified representation of K+ accumulation and clearance in the vicinity of the Ranvier node was integrated in this model.

RESULTSThe model was able to generate the following features. In the presence of 4-aminopyridine (4-AP), spike duration increased and a depolarizing afterpotential (DAP) appeared. In the presence of 4-AP and tetraethylammonium (TEA), the DAP was followed by a hyperpolarizing afterpotential (AHP) and the amplitude of this AHP increased with the frequency of the stimulation. In normal conditions (no drugs): DAP and AHP were absent after a single action potential (AP) and a short train of AP; there was a relative refractoriness in amplitude lasting for 30 ms after an AP; an early AHP was revealed by a continuous depolarizing current; and there was a partial spike adaptation for a long current step stimulus.

CONCLUSIONThe model successfully reproduced previous experiments results including long-lasting stimulation experiment, which is known to modify nerve physiological parameter values and is a key issue for visual prosthesis research.