Characterization of postischemic behavioral deficits in gerbils with and without hypothermic neuroprotection
Characterization of postischemic behavioral deficits in gerbils with and without hypothermic neuroprotection
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DOI：
10.1016/s0006-8993(98)00612-x
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发表时间：
1998-08-24
期刊：
影响因子：
2.9
通讯作者：
Sutherland, GR
中科院分区：
文献类型：
--
作者：
Colbourne, F;Auer, RN;Sutherland, GR
沙鼠全身缺血5分钟可导致海马CA1神经元延迟变性，并伴有工作记忆障碍和新环境下的多动。在这项研究中，研究人员在熟悉和陌生的环境中观察了脑后活动的特征，以确定多动是由于空间习惯受损还是另一种形式的运动多动。本研究还确定了延迟6小时的低温是否会减轻CA1神经元损伤，从而减轻功能损伤。植入脑温度探头2天后，沙鼠进行5分钟常温缺血或假手术。缺血后6小时开始冷却两组中的一组（bbb48小时）。在熟悉的笼子中测量6天的运动活动，在3个新环境中间歇性地测量第4、5和6天的活动。同时还对t型迷宫中的开放场行为和工作记忆进行了评估。未处理的缺血在第1天引起熟悉的笼子中明显的过度活跃，到第2天恢复到接近正常。尽管如此，这些沙鼠在第4-6天的新环境中表现出过度活跃。这种迷宫行为，预测海马CA1损伤，不是由于不同的习惯率或基线多动。相反，第8天的开放式野外训练显示缺血适应率下降。缺血也损害了t迷宫的工作记忆。延迟性低温使CA1区的神经元损失从81%减少到12%，减少了所有功能损伤。缺血沙鼠迅速出现自发性运动亢进，1天后恢复到接近正常。这种运动过度活跃并不能解释在新环境中延迟测试所发现的活动升高。无论如何，只有第8天的野外测试显示出类似习惯的缺陷。(C) 1998 Elsevier Science B.V.版权所有
Five minutes of global ischemia in gerbil results in delayed hippocampal CA1 neuronal degeneration, which is accompanied by working memory impairments and hyperactivity in novel environments. In this study, postischemic activity was characterized in familiar and in novel environments to determine whether hyperactivity was due to impaired spatial habituation or another form of motor hyperactivity. This study also determined whether 6-h delayed hypothermia, which reduces CA1 neuronal injury, would attenuate functional impairments. Gerbils were subjected to 5 min of normothermic ischemia or sham operation 2 days following implantation of brain temperature probes. One of two ischemic groups was cooled (> 48 h) starting at 6-h postischemia. Locomotor activity in a familiar cage was measured for 6 days while activity in three novel environments was intermittently measured on days 4, 5 and 6. Open field behavior and working memory in a T-maze were also assessed. Untreated ischemia caused marked hyperactivity in the familiar cage on day 1, which reverted to near-normal by day 2. Nonetheless, these gerbils showed hyperactivity during novel environment sessions on days 4-6. This maze behavior, which predicted hippocampal CA1 injury, was not due to different habituation rates nor baseline hyperactivity. Conversely, open field sessions on day 8 revealed ischemic habituation rate deficits. Ischemia also impaired working memory in the T-maze. Delayed hypothermia, which reduced neuronal loss in the CA1 sector to 12% from 81%, reduced all functional impairments. Ischemic gerbils quickly developed spontaneous locomotion hyperactivity that returned to near-normal after 1 day. This motor hyperactivity did not explain the elevated activity found with delayed testing in novel environments. Regardless, only the open field test on day 8 revealed a habituation-like deficit. (C) 1998 Elsevier Science B.V. All rights reserved.