ABSTRACT
Retinal prosthesis offers a potential treatment for individuals suffering from photoreceptor degeneration diseases. Establishing biological retinal models and simulating how the biological retina convert incoming light signal into spike trains that can be properly decoded by the brain is a key issue. Some retinal models have been presented, ranking from structural models inspired by the layered architecture to functional models originated from a set of specific physiological phenomena. However, Most of these focus on stimulus image compression, edge detection and reconstruction, but do not generate spike trains corresponding to visual image. In this study, based on state-of-the-art retinal physiological mechanism, including effective visual information extraction, static nonlinear rectification of biological systems and neurons Poisson coding, a cascade model of the retina including the out plexiform layer for information processing and the inner plexiform layer for information encoding was brought forward, which integrates both anatomic connections and functional computations of retina. Using MATLAB software, spike trains corresponding to stimulus image were numerically computed by four steps: linear spatiotemporal filtering, static nonlinear rectification, radial sampling and then Poisson spike generation. The simulated results suggested that such a cascade model could recreate visual information processing and encoding functionalities of the retina, which is helpful in developing artificial retina for the retinally blind.
ABSTRACT
OBJECTIVE: The 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. METHODS: The 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. RESULTS: The 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. CONCLUSION: The 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.
