Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
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DOI：
10.1186/1471-2202-11-115
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发表时间：
2010-09-14
期刊：
影响因子：
2.4
通讯作者：
Gyo, Kiyofumi
中科院分区：
文献类型：
--
作者：
Cao, Fang;Hata, Ryuji;Gyo, Kiyofumi
背景：由于缺乏可复制的啮齿动物脑干缺血模型，短暂性脑干缺血后脑干缺血损伤的时间分布尚未得到深入研究。此前，我们制作了一种可重复性的蒙古沙土鼠脑干缺血模型。结果：沙土鼠双侧椎动脉在进入颈椎横突孔前阻断双侧椎动脉形成脑干缺血。脑干缺血15min，再灌流0d(即缺血后即刻)、1d、3d、7d(每组4只)。对照组为假手术组(n=4)。沙土鼠深麻醉后，灌流固定剂进行免疫组织化学观察。微管相关蛋白2(MAP2)免疫组织化学染色检测缺血损伤。脑干缺血15min后，前庭外侧核和三叉神经脊束核腹侧可见缺血灶，再灌流后1d，缺血灶消失。然而，再灌注3d和7d后，所有动物再次出现缺血灶，并在同一区域检测到成簇的离子钙结合适配器分子-1(IBA-1)阳性细胞。结论：沙土鼠短暂性脑干缺血后，脑干发生迟发性神经细胞死亡。
Background: Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia.Results: Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals.Conclusion: These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.