EARLY EXPERIENCE AND NEURODEGENERATION

描述：早期嗅觉体验的改变可能会有深远的影响 影响在发育过程中存活的神经元的数量。增强版 在出生后早期发育的感觉体验可以诱导 嗅球神经元增多与早期嗅觉受限 刺激嗅球神经元群体中的细胞死亡。因此， 感觉刺激的变化可能诱导或抑制细胞凋亡 并影响靶组织中神经元的数量。在……里面 在其他系统中，Bcl2已被证明是一种阻止细胞凋亡的蛋白质 细胞死亡，在嗅觉本体中，bcl2的mRNA在 生后大鼠嗅球异常受限。拟议中的实验 将检验这样一种假设，即凋亡细胞死亡增加 在嗅觉受限的大鼠和小鼠幼鼠身上。其他实验将测试 假设Bcl-2蛋白在任何一种情况下都起关键作用 在发育期间保护或促进正常细胞死亡，并增加 早期嗅觉受限所致的细胞死亡。额外的实验 将检验这样一种假设，即增强过程中细胞死亡的减少 早期嗅觉体验发生在Bcl-2介导的一种机制中 蛋白质家族。

DESCRIPTION: 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.