The effect of enriched environment on the outcome of traumatic brain injury; a behavioral, proteomics, and histological study.
The effect of enriched environment on the outcome of traumatic brain injury; a behavioral, proteomics, and histological study.
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DOI：
10.3389/fnins.2011.00042
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发表时间：
2011
影响因子：
4.3
通讯作者：
Agoston DV
中科院分区：
文献类型：
--
作者：
Kovesdi E;Gyorgy AB;Kwon SK;Wingo DL;Kamnaksh A;Long JB;Kasper CE;Agoston DV
新生海马神经发生有助于创伤性脑损伤（TBI）后的功能恢复。丰富的环境（EEN）可以通过积极影响神经发生来改善TBI的结果。爆炸引起的创伤性脑损伤（bTBI）以记忆障碍和焦虑水平增加为特征，是士兵慢性残疾的主要原因。使用bTBI的啮齿动物模型，我们询问：（a）损伤后长期暴露于EEN是否可以改善行为异常和（B）EEN在分子和细胞水平以及新生神经发生上的作用。我们发现，住房受伤的动物在EEN导致显着改善空间记忆，而在正常住房（NH）的动物表现出持续的记忆障碍。VEGF和Tau蛋白而不是白细胞介素-6（IL-6）水平在EEN大鼠的背海马（DHC）中正常化，而所有三种标记物在NH大鼠中保持升高。有趣的是，在受伤后6周达到峰值后，焦虑在2个月时恢复到正常水平，与住房条件无关。在EEN中饲养动物对腹侧海马（VHC）和杏仁核（AD）中的VEGF和Tau蛋白水平没有显著影响。我们还发现EEN降低了VHC中的IL-6和IFNγ水平;这些标志物在NH后仍然升高。我们观察到的增加GFAP和DCX免疫反应性的NH动物的VHC在2个月后损伤。相反，受伤的动物住在EEN显示没有增加GFAP或DCX免疫反应在他们的VHC。总之，受伤动物长期暴露于EEN似乎对记忆功能的恢复起着积极的作用，但对焦虑没有作用，焦虑在一段时间后恢复到正常水平。EEN引起的细胞和分子变化似乎是bTBI引发的神经发生独立和依赖性恢复过程的一部分。
De novo hippocampal neurogenesis contributes to functional recovery following traumatic brain injury (TBI). Enriched environment (EEN) can improve the outcome of TBI by positively affecting neurogenesis. Blast induced traumatic brain injury (bTBI) characterized by memory impairment and increased anxiety levels, is a leading cause of chronic disability among soldiers. Using a rodent model of bTBI we asked: (a) whether long-term exposure to EEN after injury can ameliorate behavioral abnormalities and (b) what the effects of EEN are at the molecular and cellular levels and on de novo neurogenesis. We found that housing injured animals in EEN resulted in significantly improved spatial memory while animals in normal housing (NH) showed persistent memory impairment. VEGF and Tau protein but not Interleukin-6 (IL-6) levels were normalized in the dorsal hippocampus (DHC) of EEN rats while all three markers remained elevated in NH rats. Interestingly, after peaking at 6 weeks post-injury, anxiety returned to normal levels at 2 months independent of housing conditions. Housing animals in EEN had no significant effect on VEGF and Tau protein levels in the ventral hippocampus (VHC) and the amygdala (AD). We also found that EEN reduced IL-6 and IFNγ levels in the VHC; these markers remained elevated following NH. We observed an increase in GFAP and DCX immunoreactivities in the VHC of NH animals at 2 months post-injury. Conversely, injured animals housed in EEN showed no increase in GFAP or DCX immunoreactivity in their VHC. In summary, long-term exposure of injured animals to EEN appears to play a positive role in the restoration of memory functions but not on anxiety, which returned to normal levels after a significant period of time. Cellular and molecular changes in response to EEN appear to be a part of neurogenesis-independent as well as dependent recovery processes triggered by bTBI.
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影响因子：
2.9
作者：
Dihné, M;Block, F;Töpper, R
通讯作者：
Töpper, R
影响因子：
3.4
作者：
Couillard-Despres, S;Winner, B;Aigner, L
通讯作者：
Aigner, L
DOI：
10.1037/h0077579
发表时间：
1979-01-01
期刊：
JOURNAL OF COMPARATIVE AND PHYSIOLOGICAL PSYCHOLOGY
影响因子：
--
作者：
BARNES, CA
通讯作者：
BARNES, CA
影响因子：
4.2
作者：
Berrocal, Yerko;Pearse, Damien D.;Eaton, Mary J.
通讯作者：
Eaton, Mary J.
爆炸损伤引起的神经损伤的超微结构和功能特征
DOI：
10.1097/00005373-200104000-00017
发表时间：
2001-04-01
影响因子：
--
作者：
Cernak, I;Wang, ZG;Savic, J
通讯作者：
Savic, J