COGNITIVE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY PRODUCED BY CONTROLLED CORTICAL IMPACT
COGNITIVE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY PRODUCED BY CONTROLLED CORTICAL IMPACT
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DOI：
10.1089/neu.1992.9.11
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发表时间：
1992-03-01
影响因子：
4.2
通讯作者：
HAYES, RL
中科院分区：
文献类型：
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作者：
HAMM, RJ;DIXON, CE;HAYES, RL
创伤性脑损伤在人类中产生显著的认知缺陷。本实验采用实验性脑损伤的控制皮质冲击模型，采用Morris水迷宫任务研究脑损伤对空间学习记忆的影响。大鼠（n = 8）中度皮质冲击损伤（6 m/sec, 1.5 - 2.0 mm变形）。另外8只大鼠作为假受伤的对照组。在损伤后第11 ~ 15天和第30 ~ 34天评估Morris水迷宫的表现。结果显示，脑损伤大鼠在两个测试间隔的迷宫表现均有显著的缺陷（p < 0.05）。由于Morris水迷宫任务对海马体功能障碍特别敏感，本实验结果支持海马体在创伤性脑损伤后优先受到损伤的假设。这些结果表明，控制性皮质撞击性脑损伤产生与人类脑损伤后观察到的类似的持久认知缺陷。
Traumatic brain injury produces significant cognitive deficits in humans. This experiment used a controlled cortical impact model of experimental brain injury to examine the effects of brain injury on spatial learning and memory using the Morris water maze task. Rats (n = 8) were injured at a moderate level of cortical impact injury (6 m/sec, 1.5 - 2.0 mm deformation). Eight additional rats served as a sham-injured control group. Morris water maze performance was assessed on days 11 - 15 and 30 - 34 following injury. Results revealed that brain-injured rats exhibited significant deficits (p < 0.05) in maze performance at both testing intervals. Since the Morris water maze task is particularly sensitive to hippocampal dysfunction, the results of the present experiment support the hypothesis that the hippocampus is preferentially vulnerable to damage following traumatic brain injury. These results demonstrate that controlled cortical impact brain injury produces enduring cognitive deficits analogous to those observed after human brain injury.