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对沙土鼠全脑缺血2min后的脑片进行膜电位成像，研究缺血预适应对沙土鼠脑缺血耐受的影响。预适应组大鼠海马脑片兴奋性传播部分保留，而未处理组在短暂性脑缺血5min后1d兴奋传播消失。在缺血损伤2个月后，预适应动物的锥体神经元也被保存下来。结果提示，缺血预适应可诱导脑缺血耐受，从而减轻脑缺血功能障碍的程度。(2)检测了短暂缺氧缺糖状态下脑片的兴奋传递。缺氧缺糖时，大鼠海马CA1区和皮层II-III层诱发兴奋性传播减弱，但在缺氧缺糖3-5小时后部分恢复。激发传播几乎为di…暴露后1d(20~22h)，海马片中出现较多的海马片，而大脑皮层脑片中的海马片部分保存。另一方面，在氯胺酮和硫代戊醛存在的缺氧缺糖条件下，兴奋在海马和大脑皮层脑片中的传播即使在暴露后1天也能很好地保存下来。结果表明，短暂性缺氧缺糖对大鼠海马片神经元功能的损害较皮质脑片严重。一些静脉麻醉剂，如氯胺酮和硫代戊醛，可以保护神经元免受缺血时氧-葡萄糖耗竭的影响。(3)应用高速光学成像技术对三叉神经尾侧亚核(Vc)神经元兴奋的传播进行了可视化。高频刺激可在边缘层、胶状质和大细胞层引起长时间的膜去极化。这种兴奋传递被MK-801或L-703.606所抑制，提示NMDA1和NK1受体参与了Vc的伤害性传入传递。较少

(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