Various conditions lead to long-term changes in the visual cortex, if they occur during a critical period that lasts from eye opening to just before puberty. These long-term changes are controlled by electrical activity reaching the visual cortex from the two retinas, and involve elimination of some synapses and formation of others, together with changes in axon terminals. Considerable work on long-term potentiation, as well as plasticity in the visual cortex, suggests that electrical activity activates a series of steps that includes release of glutamate, activation of glutamate receptors, second messengers, protein kinases and phosphatases, transcription factors, and synthesis of proteins that are involved in synapse formation and elimination. Several substances may be involved at each step. The long-term objective of this application if to determine which substances are involved, which are not, to what degree those involved act in parallel and at which points there is a convergence of actions mediated by a single substance. This application uses the shift in ocular dominance that occurs with monocular deprivation to test a series of hypotheses: 1) that NMDA and metabotropic glutamate receptors act in parallel; 2) that protein kinase A is crucial substance upon which the actions of several substances converge (and thus that antagonists of PKA block plasticity altogether); 3) that Group II metabotropic receptors play an important role in the normal segregation of afferents from the lateral geniculate nucleus to the visual cortex.
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