Synaptic Plasticity And Neural Circuitry In The Retinal Outer Plexiform Layer: Experiments And Models

In the present work, we investigated the synaptic plasticity and neural circuitry in the outer retina using the electrophysiological method and model analysis.Firstly, in the luminosity-type horizontal cell (LHC) of isolated carp retina, we found: 1) repetitive red flashes progressively strengthened the synaptic connection between red-cone and LHC, whereas weakened that between green-cone and LHC; 2) repetitive green flashes remarkably depressed the LHC's red response, but caused little changes in the cell's green response. Lowering extracellular Ca2+ or intracellular Ca2+ in the postsynaptic neuron actually attenuated the development of activity-dependent response enhancement. Furthermore, intracellular injection of spermine or administration of ryanodine eliminated the activity-dependent response enhancement. Taking together, our data demonstrated that short-term enhancement of signal transmission to LHC might occur via calcium-dependent mechanism located atpostsynaptic neuron in a pathway-specific manner.Secondly, based on the idea that the spectral plasticity of horizontal cell may reflect some changes of synaptic efficacy between the horizontal cell and various cones, a simple quantitative model was constructed. The process consists of three components: a linear first-order dynamics, a self-excitatory component within same kind of synaptic population, and a cross-inhibitory component between different kinds of synaptic populations. It is shown that the model prediction fits reasonably well with the experimental data. An ionic channels model for LHC was developed based on Hodgkin-Huxley equations and eletrophysiological experimental results. The preliminary results suggested that calcium current might play a crucial role in response enhancement.Lastly, according to the hypothesis proposed by cascade model, the hyperpolarizing response of R/G chromaticity-type horizontal cells (R/G HCs) is driven by input directly from green cones, whereas the depolarizing response to red light is induced by the cascade signal of green cones fed back from LHCs. Light responses of R/G HCs and LHCs were intracellularly recorded in isolated superfused carp retina, and the response dynamics analyzed. These results suggest that the depolarizing response of the R/G HCs can not be entirely mediated by the negative feedback pathway from LHCs onto cones. A direct inhibitory input from red cones to R/G HCs may exist....