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Studies on the initial process of the central neuronal death by ischemia.

中枢神经元缺血死亡初始过程的研究。

基本信息

批准号：
62480470
负责人：
KATAOKA Kiyoshi
金额：
$ 0.19万
依托单位：
Ehime University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

1) An attempt was made to roughly quantify the extents of the defects of the Wijlis' ring of the mongolian gerbil. Necessary basic experiments were made on rats of single unit recording. Effect of hypothermia was studied on dogs on cerebral blood flow and on blood viscocity.2) Effect of transient ischemia on single neuronal activity and on accompanying delayed neuronal death was analyzed in CAL sector in the hippocampus of the mongolian gerbil. When the common carotid arteries were bilaterally occluded, spontaneous firing was completely disappeared within a few second. At 90 sec. occlusion, firing reappeared approximately 1 min. After the start of recirculation in a manner of burst with 30 - 100 Hz, which lasted for 10 - 40 min. No cell death was observed in these cases. At 5 min. occlusion, on the other hand, the rate of firing reappearing approximately 15 min. after recirculation, never exceeded the preocclusion level (5 - 10 Hz). The cell death was accompanied in approximately 30 % of animals of this group. In separate experiments, extracellular concentration of glutamic acid was estimated using microdialysis perfusion method and by enzyme cycling procedures. Shortly after the carotid occlusion, a raised concentration of the amino acid was consistently observed. Thus, it was concluded that delaved neuronal death was not induced solely by burst firing or glutamic acid neurotoxicity.

1)对蒙古沙鼠Wijlis环的缺陷程度进行了粗略的量化。在单单位记录大鼠身上进行必要的基础实验。研究了低温对狗脑血流量和血液粘度的影响。2)分析了短暂性缺血对蒙古沙鼠海马CAL区单个神经元活动及伴随的延迟性神经元死亡的影响。当双侧颈总动脉闭塞时，自发放电在数秒内完全消失。在90秒闭塞时，约1分钟再次出现射击。再循环开始后，以30 - 100赫兹的爆发方式进行，持续10 - 40分钟。在这些病例中未观察到细胞死亡。另一方面，在闭塞5分钟时，再循环后约15分钟再次出现的放电率从未超过闭塞前水平（5 - 10 Hz）。该组中约30%的动物伴有细胞死亡。在单独的实验中，利用微透析灌注法和酶循环程序估计谷氨酸的细胞外浓度。在颈动脉闭塞后不久，持续观察到氨基酸浓度升高。因此，我们认为，不完全是由突发放电或谷氨酸神经毒性引起的神经元死亡。