A change in early olfactory experience can have profound affects on the number of neurons that survive during development. Enhanced sensory experience during early post-natal development can induce an increase in olfactory bulb neurons, and early olfactory restriction stimulates cell death in a population of olfactory bulb neurons. Thus, changes in sensory stimulation may induce or suppress apoptosis during development and influence the number of neurons in target tissues. In other systems, Bcl-2 has been shown to be a protein that blocks apoptotic cell death, and in the olfactory bulk, the mRNA for BCL-2 is elevated in oder-restricted postnatal rat olfactory bulbs. The proposed experiments will test the hypothesis that there is an increase in apoptotic cell death in odor-restricted rat and mouse pups. Other experiments will test the hypothesis that the Bcl-2 protein plays a critical role in either protecting or promoting normal cell death during development and increased cell death induced by early olfactory restriction. Additional experiments will test the hypothesis that a reduction in cell death during enhanced early olfactory experience occurs during a mechanism mediated by the Bcl-2 protein family.
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