Synaptic competition in developmental binocular plasticity.
A mathematical model of the possible physiological and biochemical mechanisms responsible for the changes occurring during binocular development is proposed. The model is based on the mechanisms postulated for the occurrence of well known plastic processes, such as post-tetanic potentiation, sensitization and heterosynaptic inhibition. Because all these processes are of presynaptic nature, we have postulated that the plastic processes occurring during development are of the same nature. The factors we have considered in our model are: the transmitter pool size, the mobilization or synthesis of the transmitter, the transmitter release by the physiological stimulus, the neuroendocrine and genetic activity. With this model we have simulated the following phenomena during ocular development: (1) normal binocular development; (2) monocular deprivation, including the effects of reversing the occluded eye; (3) binocular deprivation and recovery; and (4) effects of alternating deprivation on mature binocularity. The model also allows us to explain in a natural way the possible changes occurring during denervation or disuse.
D000818:Animals; D005075:Biological Evolution; D002415:Cats; D008959:Models, Neurological; D009433:Neural Inhibition; D018377:Neurotransmitter Agents / Q000502:physiology; D012683:Sensory Deprivation; D013569:Synapses / Q000502:physiology; D014785:Vision, Ocular; D014793:Visual Cortex / Q000254:growth & development*
D018377:Neurotransmitter Agents