RADIAL GLIA AND CAJAL RETZIUS CELLS IN NEURON MIGRATION

神经元迁移中的放射状胶质细胞和 CAJAL RETZIUS 细胞

• 批准号: 6530923
• 负责人: SHARON L JULIANO
• 金额: $ 25.45万
• 依托单位: HENRY M. JACKSON FDN FOR THE ADV MIL/MED
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-03-15 至 2006-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6530923
• 关键词: antimitotics; cell differentiation; cell migration; developmental neurobiology; disease /disorder model; embryo /fetus tissue /cell culture; ferrets; glia; laboratory mouse; morphology; neocortex; neurons; tissue /cell culture; vertebrate embryology

DESCRIPTION: (Adapted from the Investigator's Abstract) The proposed research utilizes a model of impaired neurodevelopment in the ferret that presents as a thin and disrupted cerebral cortex, with ectopic clusters of cells typical of cortical dysplasia. During generation of the earliest born neocortical layers, treatment with the antimitotic agent, methylazoxy methanol (MAM), disrupts radial glia, and results in abnormally situated Cajal Retzius cells. Features of the brain resulting from this treatment are an excellent model for study of migration defects. The current proposal investigates the following questions resulting from this model. (1) What causes the radial glia to become disorganized? (2) What prevents cells from migrating effectively into the neocortex? (3) What causes the Cajal Retzius cells to become disorganized? The hypothesis is that a radialization factor is present in normal cortex, and when it is provided to MAM-treated cortex, normal radial glial morphology can be restored. A second, related hypothesis is that the restoration of normal radial glial morphology can improve migration in MAM-treated cortex. These hypotheses will be tested and the biochemical nature of the radialization factor will be defined using organotypic and cell cultures and migration bioassays to analyze this system.

描述：（根据调查员的摘要进行了改编） 拟议的研究利用了神经发育受损模型 雪貂作为稀薄且干扰的大脑皮层，异位 皮质发育不良的典型细胞簇。在一代 最早出生的新皮层层，用抗魔法剂治疗， 甲基氧基甲醇（MAM），破坏radial胶质细胞纤维，并异常导致 位于Cajal retzius细胞。由此产生的大脑的特征 治疗是研究迁移缺陷的绝佳模型。电流 提案研究了该模型引起的以下问题。 （1） 是什么导致径向神经胶质发生混乱？ （2）什么阻止了细胞 从有效迁移到新皮层？ （3）是什么原因导致Cajal retzius细胞变得混乱？假设是辐射化 因子存在于正常皮质中，并且提供给MAM处理的因子 皮质，正常的径向神经胶质形态可以恢复。第二，相关 假设是恢复正常的径向神经胶质形态可以 改善MAM处理的皮质的迁移。这些假设将进行检验，并且 辐射因子的生化性质将使用 器官和细胞培养物以及迁移生物测定以分析该系统。