HYPOXIA OF BRAIN TISSUE SLICES

脑组织切片缺氧

• 批准号: 2037099
• 负责人: GEORGE G SOMJEN
• 金额: $ 26.74万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1982
• 资助国家: 美国
• 起止时间: 1982-07-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2037099
• 关键词: calcium flux; cell osmotic pressure; cerebral ischemia /hypoxia; confocal scanning microscopy; hippocampus; ion transport; laboratory rat; membrane permeability; membrane potentials; sodium ion; spreading cortical depression; voltage /patch clamp

DESCRIPTION (Applicant's Abstract): Interrupted supply of oxygen is the main cause of neuron injury in cerebral stroke and transient cerebral ischemia. The long-range goal of this project is a comprehensive study of the acute effects of hypoxia on central nervous tissue of mammals. Hypoxic failure of cerebral function takes place in a succession of ell defined stages. First synaptic transmission is depressed, then cells lose membrane potential, release much of their potassium and take up sodium, chloride, calcium and water. Timely reoxygenation is still followed by recovery of neuron function, but if the depolarized state continues too long, injury becomes irreversible. In the past this laboratory has contributed to the understanding of each of these hypoxic changes. The goal for the present application is the biophysical mechanism of the hypoxic depolarization. Several hypotheses are proposed to explain the increased permeability of the neuronal membranes that result in the profound depolarization and transmembrane ion exchanges. The validity of these proposals will be tested with a variety techniques, including: Recording of ion changes in interstitial space of cerebral tissue slices; whole-cell recordings from neurons in brain tissue slices; single-channel recording from cell-attached patches; imaging of the intrinsic optical changes of cerebral tissue during hypoxia; confocal fluorescence microscopic imaging of intracellular calcium activity of cells in tissue slices. Besides neurons, the role of glial cells will also be studied.

描述（申请人的摘要）：氧气供应中断是 脑卒中和短暂性脑梗死神经元损伤的主要原因 缺血 该项目的长期目标是全面研究 缺氧对哺乳动物中枢神经组织的急性影响。 脑功能的减退性衰竭是在一系列的脑损害中发生的， 明确的阶段。 首先突触传递受到抑制，然后细胞失去 膜电位，释放大量的钾并吸收钠， 氯化物、钙和水。 及时复氧仍是其次 神经元功能的恢复，但如果去极化状态也继续下去， 长了，伤害就不可逆转了。 在过去，这个实验室 有助于理解每一种缺氧变化。 目标 本申请的目的是缺氧性脑缺血的生物物理机制。 去极化 提出了几种假设来解释渗透性的增加， 导致深度去极化的神经元膜， 跨膜离子交换 这些建议的有效性将受到考验 用各种技术，包括：记录离子变化， 脑组织切片的间质空间;来自 脑组织切片中的神经元;细胞贴附的单通道记录 补丁;成像的内在光学变化的脑组织在 缺氧;细胞内钙离子共聚焦荧光显微成像 组织切片中细胞的活性。 除了神经元，胶质细胞的作用 细胞也将被研究。