Exploration of plasticity visual physiologic functions by simultaneous studies on artificial neural networks and vertebrate retina

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Physiological experiments as well as computational studies were conducted to explore certain aspects of the neural plasticity. Due to the lack of space, this report only describes our results concerned with synaptic plasticity mechanisms in the vertebrate retina which morphogenetically is a part of the brain. Thus, we have established that the synapse from short-lambda (wavelength) sensitive cones to H1 type horizontal cells (H1 HCs) is different from the excitatory (sign-conserving) synapse mediating the long-lambda visual signal transmission, althogh both synapses presumablly use L-glutamate as the neurotransmitter ; the short-lambda synapse is sigh-inverting and conductance-decreasing with APB as an agonist, and the synapse is metabotropic with cGMP as the second messenger. Furthermore, No (nitric oxide) is involved in the molecular mechanism, by facilitating the cGMP production when the retina is light adapted. This explains the fact that the short-lambda synapse is dormant during dark adaptation. In fact, light adaptaion and No have the same effects on H1 HCs in sharpening the spectral sensitivity curve and increasing the receptive field size for red than blue lights. These observations were succesfully accounted for by a cable theory model incorporating the polarity-inverting and conductance-decreasing properties of the short-lambda synapse.