Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats
Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats
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DOI：
10.1016/s0306-4522(98)00142-0
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发表时间：
1998-11-01
期刊：
影响因子：
3.3
通讯作者：
McIntosh, TK
中科院分区：
文献类型：
--
作者：
Pierce, JES;Smith, DH;McIntosh, TK
临床研究已经证明，患者在创伤性脑损伤后持续长时间的行为缺陷，在某些情况下最终导致阿尔茨海默病的认知和组织病理学特征。然而，很少有研究检查实验性创伤性脑损伤的长期后果。在本研究中，对麻醉的雄性Sprague-Dawley大鼠（n=185）进行严重的侧向液压冲击脑损伤（n=115）或假损伤（n=70），并在损伤后1年评价认知和神经功能缺损以及组织病理学变化。与假损伤对照组相比，脑损伤动物表现出空间学习障碍，并持续到伤后一年。此外，特定神经运动功能任务的缺陷也持续到伤后一年。使用多种抗体的淀粉样前体蛋白和/或淀粉样前体蛋白样蛋白的免疫组化显示新的轴突变性在纹状体，胼胝体和受伤的皮质损伤后长达一年，在丘脑损伤后长达六个月。损伤脑的组织学评估显示皮质腔的进行性扩张、侧脑室的扩大、海马的变形和丘脑的钙化，这些结果表明实验性创伤性脑损伤可导致长期的认知和神经运动功能障碍，并伴有持续的神经退行性变。(C)1998年IBRO。出版社：Elsevier Science Ltd
Clinical studies have demonstrated that patients sustain prolonged behavioral deficits following traumatic brain injury, in some cases culminating in the cognitive and histopathological hallmarks of Alzheimer's disease. However, few studies have examined the long-term consequences of experimental traumatic brain injury. In the present study, anesthetized male Sprague-Dawley rats (,n=185) were subjected to severe lateral fluid-percussion brain injury (n=115) or sham injury (n=70) and evaluated up to one year post-injury for cognitive and neurological deficits and histopathological changes. Compared with sham-injured controls, brain-injured animals showed a spatial learning impairment that persisted up to one year post-injury. In addition, deficits in specific neurologic motor function tasks also persisted up to one year post-injury. Immunohistochemistry using multiple antibodies to the amyloid precursor protein and/or amyloid precursor protein-like proteins revealed novel axonal degeneration in the striatum, corpus callosum and injured cortex up to one year post-injury and in the thalamus up to six months post-injury. Histologic evaluation of injured brains demonstrated a progressive expansion of the cortical cavity, enlargement of the lateral ventricles, deformation of the hippocampus, and thalamic calcifications.Taken together, these findings indicate that experimental traumatic brain injury can cause long-term cognitive and neurologic motor dysfunction accompanied by continuing neurodegeneration. (C) 1998 IBRO. Published by Elsevier Science Ltd.