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New development of basic study on protection of ischemic brain edema and neuronal dysfunction using brain slice model

脑切片模型保护缺血性脑水肿和神经元功能障碍的基础研究新进展

基本信息

批准号：
12470317
负责人：
FUJIWARA Naoshi
金额：
$ 9.15万
依托单位：
NIIGATA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

项目摘要

(1) Ischemic tolerance induced by ischemic preconditioning was investigated by applying a membrane potential imaging technique to brain slices of gerbils, which were pretreated with 2-min forebrain ischemia. Excitation propagation in hippocampal slices of preconditioned animals was partially preserved, while that of untreated animals disappeared 1 day after 5-min transient ischemia. Pyramidal neurons of preconditioned animals were also preserved 2 months after the ischemic insult. The results suggest that ischemic preconditioning induced ischemic tolerance to reduce the extent of ischemic functional disturbance.(2) Excitation propagation in brain slices, which were transiently exposed to oxygen-glucose deprivation, was examined. Evoked excitation propagation in the hippocampal CA1 and cortical layer II-III were diminished during exposure to oxygen-glucose deprivation, but partially recovered 3-5 hr after 5-min exposure to oxygen-glucose deprivation. The excitation propagation almost di … More sappeared in hippocampal slices 1 day (20-22 hr) after the exposure, while that in cortical slices was partially preserved. On the other hand, excitation propagation in both hippocampal and cortical slices, which were exposed oxygen-glucose deprivation in the presence of ketamine and thiamylal, well preserved even 1 day after the exposure. The results indicate that neuronal function in hippocampal slices more severely damaged than that in cortical slices by transient exposure to oxygen-glucose deprivation. Some intravenous anesthetics, e.g. ketamine and thiamylal, may protect neurons from oxygen-glucose depletion during ischemia.(3) Propagation of neuronal excitation in the trigeminal subnucleus caudalis (Vc) was visualized using a high-speed optical imaging technique applied to medulla slice preparations. High frequency stimulation induced long-lasting membrane depolarization in the marginal layer, substantia gelatinosa and magnocellular layer. This excitation propagation was suppressed by MK-801 or L-703.606, suggesting that NMDA- and NK_1-receptors are involved in the nociceptive afferent transmission in Vc. Less

(1)通过对沙鼠脑切片应用膜电位成像技术，研究缺血预处理诱导的缺血耐受性，沙鼠脑切片经过2分钟的前脑缺血预处理。经预处理的动物海马切片中的兴奋传播部分保留，而未处理的动物的兴奋传播在5分钟短暂缺血后1天消失。预处理动物的锥体神经元在缺血性损伤后两个月也被保存。结果表明，缺血预处理诱导缺血耐受，从而减轻缺血功能障碍的程度。(2)检测了短暂暴露于氧糖剥夺的脑切片中的兴奋传播。海马 CA1 和皮质层 II-III 中的诱发兴奋传播在暴露于氧-葡萄糖剥夺期间减弱，但在暴露于氧-葡萄糖剥夺 5 分钟后 3-5 小时部分恢复。暴露后 1 天（20-22 小时），海马切片中的激发传播几乎消失，而皮质切片中的激发传播则部分保留。另一方面，在存在氯胺酮和硫淀粉醛的情况下暴露于氧-葡萄糖剥夺的海马和皮质切片中的兴奋传播甚至在暴露后1天也保存完好。结果表明，由于短暂暴露于氧-葡萄糖剥夺，海马切片中的神经元功能比皮质切片中的神经元功能受损更严重。一些静脉麻醉剂，例如氯胺酮和硫淀粉醛可以保护神经元在缺血期间免受氧葡萄糖消耗。(3) 使用应用于髓质切片制备的高速光学成像技术来可视化三叉神经尾亚核 (Vc) 中神经元兴奋的传播。高频刺激诱导边缘层、胶质质和大细胞层的持久膜去极化。这种兴奋传播被 MK-801 或 L-703.606 抑制，表明 NMDA- 和 NK_1- 受体参与 Vc 中的伤害性传入传递。较少的