ISCHEMIC TOLERANCE DEPRESSED INIRACELLULAR CALCIUM ELEVATION IN GERBILHIPPOCAMPUS

沙鼠海马缺血耐受性降低细胞内钙升高

• 批准号: 10680749
• 负责人: SHIMAZAKI Kuniko
• 金额: $ 2.18万
• 依托单位: Jichi Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10680749/
• 关键词: Bcl-2; apoptosis; gerbil; hippocampus; brain ischermia; adeno-associated virus vecoor; delayed neuronal death; 遅発性神経細胞死; GLT-1

In the gerbil hippocampus, a short (2mim) sublethal ischemic episode preceding lethal (5mim) ischemia is known to increase tolerance against death in CA1 pyramydal neurons. Intracellular calcium elevation level after exposing to the anoxic-aglycemic medium (95%NィイD22ィエD2/5%C0ィイD22ィエD2, glucose-free) in the rhod-2-loaded hippocampal slices was compared between ischemia-tolerant and non-tolerant gerbils. In non-tolerant gerbils, after switching the normal ringer to anoxic-aglycemic medium an abrupt increase in fluorescence in the Ca1area was seen. Thereafter, a steady increase in intracellular calcium took place with the peak fluorescence intensity at nearly 3 times of the base line. In ischemia-tolerant gerbils, however, the fluorescence increase stayed at significantly lower level than non-tolerant gerbils. Tolerance for ischema was known to be acquired from 1 to 7 days after 2 min ischemia but after 14 days no protective effect was observed. Pretreatment with 1 min ischemia was found to be too brief to induce tolerance. In agreement with these data, magnitude of fluorescence elevation in gerbils at 14 days after 2 min ischemia and at 2 days after 1 min ischemia were almost the same as in the non-tolerant gerbils. Our results suggest that conditioning sublethal ischemia induced to tolerance for ischemic neuronal death which is deeply related to acute increase in intracellular calcium.

在沙鼠海马中，致死性（5 mim）缺血前的短暂（2 mim）亚致死性缺血发作可增加CA 1海马神经元对死亡的耐受性。在缺血耐受和不耐受的沙土鼠海马脑片中，比较暴露于无氧无糖培养基（95%N谷氨酸D22谷氨酸D2/5%C谷氨酸D22谷氨酸D2，无葡萄糖）后细胞内钙升高水平。在不耐受的沙鼠中，将正常铃声切换到缺氧-无血糖培养基后，观察到Ca 1区域的荧光突然增加。此后，细胞内钙稳定增加，峰值荧光强度接近基线的3倍。然而，在缺血耐受沙鼠中，荧光增加保持在显著低于非耐受沙鼠的水平。已知缺血耐受性在2分钟缺血后1至7天获得，但在14天后未观察到保护作用。缺血1分钟的预处理时间太短，不能诱导耐受。与这些数据一致，沙鼠在2分钟缺血后14天和1分钟缺血后2天的荧光升高幅度与非耐受沙鼠几乎相同。我们的研究结果表明，条件性亚致死性缺血诱导耐受缺血性神经元死亡，这是深相关的急性细胞内钙增加。

项目成果

Kuniko Shimazaki et al: "Ischemic tolerance depressed intracellular calcium elevation in gerbil hippocampus"Society for Neuroscience abstract. 24. 218 (1998)

Kuniko Shimazaki 等人：“缺血耐受抑制了沙鼠海马细胞内钙的升高”神经科学学会摘要。

Kuniko Shimazaki et al: "Bcl-2 protects late stage of delayed neuronal death of hippocampal CA1 cells after ischemia"Soc Neurosci Abstr. 25. 1583 (1999)

Kuniko Shimazaki 等人：“Bcl-2 保护缺血后海马 CA1 细胞延迟性神经元死亡的晚期”Soc Neurosci Abstr。

島崎久仁子他: "アデノ随伴ウイルスベクターによる海馬神経細胞への遺伝子導入"脳21. 2(3). 45-51 (1999)

Kuniko Shimazaki 等人：“使用腺相关病毒载体将基因转移到海马神经元”Brain 21. 2(3) (1999)。

Kuniko Shimazaki et al.: "Ischemic to lerance depressed intracellular calcium elevation in gerbil hippocampus." Society for Neuroscience dostroct. 28. 218 (1998)

Kuniko Shimazaki 等人：“缺血性耐受性降低了沙鼠海马细胞内钙的升高。”

Hiroyuki Cho et al: "Biphasic changes in F3/Contactin expression in the gerbil hippocampus after transient ischemia"Experimental Brain Research. 122. 227-234 (1998)

Hiroyuki Cho 等人：“短暂性缺血后沙鼠海马中 F3/Contactin 表达的双相变化”实验脑研究。