HYPOXIA OF BRAIN TISSUE SLICES

脑缺氧或脑缺血导致I.可逆性突触衰竭 传递；II.神经元功能不可逆转的丧失，指示细胞 损伤；III.最初短暂恢复后的延迟恶化 在复氧之后。这个实验室之前的研究已经处理了 所有三个阶段的不同方面。本申请是 主要致力于神经元失去能力的机制 从缺氧性侮辱中恢复过来。 这项计划的长远目标是全面研究 低氧对哺乳动物中枢神经组织的影响。自.以来 目的是将缺氧本身的影响与 间接影响和全身变化，使用体外制剂。在……里面 在这个续订期间，我们将集中讨论 海马区从可逆性缺氧到不可逆性缺氧的转变 组织切片。从我们以前的工作中得出的几个假设是 测试过。记录技术包括传统的微电极、离子 选择性微电极，以及全细胞配置的膜片钳。 拟议的实验将涵盖以下主题： L。pH对缺氧性扩散性抑郁(SD)样症状的影响 去极化，以及从缺氧的影响中恢复。 2.低氧时间质间隙的变化及细胞的作用 缺氧性SD样除极肿胀。 3.高渗和低渗介质与低氧的相互作用。 4.渗透细胞膜对单价阳离子的影响 海马片。 5.与CA1恢复能力丧失相关的膜变化 海马区脑片锥体神经元的免疫组织化学研究 全细胞结构的密封膜片钳。

Cerebral hypoxia or ischemia leads to I. reversible failure of synaptic transmission; II. irreversible loss of neuron function, indicating cell injury; III. delayed deterioration after initial transient recovery following reoxygenation. Previous research in this laboratory has dealt with various aspects of all three phases. The present application is devoted mainly to the mechanism by which neurons lose the capacity to recover from hypoxic insult. The long-range goal of this project is a comprehensive study of the acute effects of hypoxia on central nervous tissue of mammals. Since the objective is the effect of oxygen deprivation itself separated from indirect effects and systemic changes, in vitro preparations are used. In this renewal period we will concentrate on the mechanism and causes of the transition from reversible to irreversible hypoxic change in hippocampal tissue slices. Several hypotheses derived from our previous work will be tested. Recording techniques include conventional microelectrodes, ion selective microelectrodes, and patch-clamping in whole-cell configuration. The proposed experiments will cover the following topics: l. The effects of pH on hypoxic spreading depression (SD)-like depolarization, and on recovery from the effects of hypoxia. 2. Changes of interstitial space during hypoxia, and the role of cell swelling in hypoxic SD-like depolarization. 3. Interaction of hyper-osmotic and hypo-osmotic media with hypoxia. 4. Effects of permeabilizing cell membranes to monovalent cations in hippocampal slices. 5. Membrane changes associated with loss of recovery capacity in CA1 pyramidal neurons in hippocampal tissue slices, investigated with tight seal patch-clamping in whole-cell configuration.