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

Research Project

Project/Area Number	62480470
Research Category	Grant-in-Aid for General Scientific Research (B)
Allocation Type	Single-year Grants
Research Field	Neurophysiology and muscle physiology
Research Institution	Ehime University
Principal Investigator	KATAOKA Kiyoshi Ehime University, Professor, 医学部, 教授 (20025589)
Co-Investigator(Kenkyū-buntansha)	MITANI Akira Ehime University, Instructer, 医学部, 助手 (50200043) KUSUZAKI Kosaku Ehime University, Instructer, 医学部, 助手 (70093929)
Project Period (FY)	1987 – 1988
Project Status	Completed (Fiscal Year 1988)
Budget Amount *help	¥300,000 (Direct Cost: ¥300,000) Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Keywords	Mongolian gerbil / Willis' ring defect / Hippocampus / Unit recording / ischemia / Delayed neuronal death / 海馬CAl領域 / 遅発性ニューロン死 / 砂ネズミ / 脳底動脈輪形成不全 / 海馬CALニューロン / 単一ニューロン自発放電 / グルタミン酸神経毒性 / ラット / 自発性発火頻度 / 犬 / 低温脳循環
Research Abstract	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.