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首页> 外文期刊>Journal of neuroinflammation >Traumatic axonal injury in the mouse is accompanied by a dynamic inflammatory response, astroglial reactivity and complex behavioral changes
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Traumatic axonal injury in the mouse is accompanied by a dynamic inflammatory response, astroglial reactivity and complex behavioral changes

机译：小鼠创伤性轴突损伤伴随动态炎症反应，星形胶质细胞反应性和复杂的行为变化

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Background Diffuse traumatic axonal injury (TAI), a common consequence of traumatic brain injury, is associated with high morbidity and mortality. Inflammatory processes may play an important role in the pathophysiology of TAI. In the central fluid percussion injury (cFPI) TAI model in mice, the neuroinflammatory and astroglial response and behavioral changes are unknown. Methods Twenty cFPI-injured and nine sham-injured mice were used, and the neuroinflammatory and astroglial response was evaluated by immunohistochemistry at 1, 3 and 7 days post-injury. The multivariate concentric square field test (MCSF) was used to compare complex behavioral changes in mice subjected to cFPI (n = 16) or sham injury (n = 10). Data was analyzed using non-parametric statistics and principal component analysis (MCSF data). Results At all post-injury time points, β-amyloid precursor protein (β-APP) immunoreactivity revealed widespread bilateral axonal injury and IgG immunostaining showed increased blood–brain barrier permeability. Using vimentin and glial fibrillary acidic protein (GFAP) immunohistochemistry, glial cell reactivity was observed in cortical regions and important white matter tracts peaking at three days post-injury. Only vimentin was increased post-injury in the internal capsule and only GFAP in the thalamus. Compared to sham-injured controls, an increased number of activated microglia (MAC-2), infiltrating neutrophils (GR-1) and T-cells (CD3) appearing one day after TAI (P<0.05 for all cell types) was observed in subcortical white matter. In the MCSF, the behavioral patterns including general activity and exploratory behavior differed between cFPI mice and sham-injured controls. Conclusions Traumatic axonal injury TAI resulted in marked bilateral astroglial and neuroinflammatory responses and complex behavioral changes. The cFPI model in mice appears suitable for the study of injury mechanisms, including neuroinflammation, and the development of treatments targeting TAI.
机译：背景弥漫性创伤性轴索损伤（TAI）是颅脑损伤的常见后果，与高发病率和高死亡率相关。炎症过程可能在TAI的病理生理中起重要作用。在小鼠的中枢性脑震荡损伤（cFPI）TAI模型中，神经炎症和星形胶质反应以及行为改变尚不清楚。方法采用20只cFPI损伤的小鼠和9只假损伤的小鼠，在损伤后1、3和7天通过免疫组织化学方法评估其神经炎症和星形胶质细胞反应。多元同心方场检验（MCSF）用于比较遭受cFPI（n = 16）或假伤（n = 10）的小鼠的复杂行为变化。使用非参数统计和主成分分析（MCSF数据）分析数据。结果在所有损伤后的时间点，β-淀粉样蛋白前体蛋白（β-APP）的免疫反应性显示出广泛的双侧轴突损伤，IgG免疫染色显示血脑屏障通透性增加。使用波形蛋白和神经胶质纤维酸性蛋白（GFAP）免疫组织化学，在皮层区域观察到神经胶质细胞反应性，重要的白质束在损伤后三天达到峰值。内囊损伤后仅波形蛋白升高，丘脑中仅GFAP升高。与假手术受伤的对照组相比，观察到TAI后一天出现的活化小胶质细胞（MAC-2），浸润性中性粒细胞（GR-1）和T细胞（CD3）数量增加（对于所有细胞类型，P <0.05）皮质下白质。在MCSF中，cFPI小鼠和假伤对照组之间的行为模式（包括一般活动和探索行为）有所不同。结论创伤性轴索损伤TAI导致明显的双侧星形胶质和神经炎症反应以及复杂的行为改变。小鼠中的cFPI模型似乎适合研究损伤机制，包括神经炎症和开发针对TAI的疗法。

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