MK-801, BUT NOT ANISOMYCIN, INHIBITS THE INDUCTION OF TOLERANCE TO ISCHEMIA IN THE GERBIL HIPPOCAMPUS
MK-801, BUT NOT ANISOMYCIN, INHIBITS THE INDUCTION OF TOLERANCE TO ISCHEMIA IN THE GERBIL HIPPOCAMPUS
复制标题
DOI：
10.1016/0304-3940(92)90871-4
复制
发表时间：
1992-05-11
影响因子：
2.5
通讯作者：
KOGURE, K
中科院分区：
文献类型：
--
作者：
KATO, H;LIU, Y;KOGURE, K
我们检测了N-甲基-D-天冬氨酸(NMDA)受体拮抗剂MK-801或可逆性蛋白质合成抑制剂山奈素是否能抑制亚致死性脑缺血预适应后沙土鼠海马区缺血耐受的诱导。缺血2min进行预适应。诱导热休克蛋白-72免疫反应，防止3d后3min脑缺血所致的海马CA1神经元损伤。MK-801抑制耐受诱导，但两组热休克蛋白合成均减少。结果提示，NMDA受体的激活引起应激反应，从而诱导缺血耐受。
We examined whether MK-801, an N-methyl-D-aspartate (NMDA)-receptor antagonist, or anisomycin, a reversible protein synthesis inhibitor, inhibits thc induction of ischemic tolerance following preconditioning with sublethal ischemia in gerbil hippocampus. Preconditioning with 2 min of ischemia. which induced heat shock protein-72 immunoreactivity, prevented hippocampal CA1 neuronal damage following 3 min of ischemia produced 3 days later. MK-801, but not anisomycin, inhibited the induction of tolerance although the heat shock protein synthesis was reduced in both groups. The present result suggests that NMDA receptor activation, causing stress response, induces the ischemic tolerance.