EARLY EXPERIENCE AND NEURODEGENERATION

描述：早期嗅觉体验的变化可能会产生深远的影响。 影响发育过程中存活的神经元数量。增强 出生后早期发育过程中的感觉经历可以诱导 嗅球神经元增加和早期嗅觉限制 刺激嗅球神经元的细胞死亡。因此，在本发明中， 感觉刺激的变化可以诱导或抑制细胞凋亡， 发育并影响靶组织中神经元的数量。在 在其他系统中，Bcl-2已被证明是一种阻断凋亡的蛋白质， 细胞死亡，并且在嗅觉体中，BCL-2的mRNA在 嗅觉受限的出生后大鼠嗅球。拟议的实验 将检验凋亡性细胞死亡增加的假设， 在气味受限的大鼠和小鼠幼崽中。其他实验将测试 假设Bcl-2蛋白在以下两个过程中起着关键作用： 保护或促进发育过程中的正常细胞死亡， 早期嗅觉限制诱导的细胞死亡。另外的实验 将测试一个假设，即在增强的细胞死亡减少， 早期嗅觉体验发生在Bcl-2介导的机制中， 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.