The goal of the proposed experiments is to understand the mechanisms and rules which govern modification of synaptic strength in the cerebral cortex throughout life. Five hypotheses are proposed. First, the cortical depression mechanisms are active not passive. To address this question, changes in neuronal activity in vibrissa representation in the barrel cortex caused by uni- vibrissa deprivation (removing all but a single vibrissa) will be studied. Second, cortical depression mechanisms are caused by heterosynaptic interactions. To address the hypothesis, cortical activity will be studied and compared in animals with a single vibrissa deprived and all vibrissae are deprived. Third, cortical potentiation mechanisms are associated not competitive in adults and adolescents. Forth, cortical potentiation mechanisms require CAMKII in adults but not adolescents. Fifth, long term changes in cortical plasticity require protein synthesis via CREB. In these two sets of experiments, the mouse barrel cortical activities of CAMKII and CREB knockout mice will be investigated.
