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

(1)应用膜电位成像技术观察了沙土鼠脑缺血预处理诱导的缺血耐受。预处理动物海马切片的兴奋传播部分保存，而未处理的动物在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损伤后2个月也被保留。结果提示，缺血预处理可诱导缺血耐受，减轻缺血功能障碍。(2)在大脑切片，这是短暂暴露于氧-葡萄糖剥夺，兴奋传播进行了检查。在海马CA 1区和皮层II-III层的诱发兴奋传播减少暴露期间，以氧-葡萄糖剥夺，但部分恢复3-5小时后5分钟暴露于氧-葡萄糖剥夺。激发传播几乎停止 ...更多信息 海马脑片在照射后1d（20-22小时）出现明显的荧光，而皮层脑片则部分保留。另一方面，兴奋传播在海马和皮层切片，暴露氧-葡萄糖剥夺在氯胺酮和thiamylal的存在下，保存良好，甚至1天后曝光。结果表明，短暂缺糖缺氧对海马脑片神经元功能的损害比皮层脑片更为严重。一些静脉麻醉剂，如氯胺酮和硫代戊醛，可以保护神经元在缺血期间免受氧-葡萄糖耗尽。(3)三叉神经尾侧亚核（Vc）的神经元兴奋的传播可视化使用高速光学成像技术应用于髓质切片制备。高频刺激在边缘层、胶状质和大细胞层引起持续时间较长的膜去极化。MK-801或L-703.606可抑制这种兴奋传递，提示NMDA和NK_1受体参与Vc伤害性传入传递。少

(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