EARLY EXPERIENCE AND NEURODEGENERATION

早期经历和神经退行性变

• 批准号: 6523460
• 负责人: Michael Leon
• 金额: $ 32.19万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-09-01 至 2003-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6523460
• 关键词: BCL2 gene /protein; animal genetic material tag; apoptosis; developmental genetics; developmental neurobiology; early experience; gene induction /repression; genetically modified animals; infant animal; laboratory mouse; laboratory rat; neural degeneration; neural plasticity; neurogenetics; neurons; odors; olfactory lobe; olfactory stimulus

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.

早期嗅觉体验的改变会产生深远的影响