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首页> 外文期刊>The European Journal of Neuroscience >Diffuse traumatic axonal injury in mice induces complex behavioural alterations that are normalized by neutralization of interleukin-1
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Diffuse traumatic axonal injury in mice induces complex behavioural alterations that are normalized by neutralization of interleukin-1

机译：弥漫性创伤性轴突损伤在小鼠中诱导复杂的行为改变，可通过中和白细胞介素1来正常化

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摘要

Widespread traumatic axonal injury (TAI) results in brain network dysfunction, which commonly leads to persisting cognitive and behavioural impairments following traumatic brain injury (TBI). TBI induces a complex neuroinflammatory response, frequently located at sites of axonal pathology. The role of the pro-inflammatory cytokine interleukin (IL)-1 has not been established in TAI. An IL-1-neutralizing or a control antibody was administered intraperitoneally at 30min following central fluid percussion injury (cFPI), a mouse model of widespread TAI. Mice subjected to moderate cFPI (n=41) were compared with sham-injured controls (n=20) and untreated, naive mice (n=9). The anti-IL-1 antibody reached the target brain regions in adequate therapeutic concentrations (up to similar to 30g/brain tissue) at 24h post-injury in both cFPI (n=5) and sham-injured (n=3) mice, with lower concentrations at 72h post-injury (up to similar to 18g/g brain tissue in three cFPI mice). Functional outcome was analysed with the multivariate concentric square field (MCSF) test at 2 and 9days post-injury, and the Morris water maze (MWM) at 14-21days post-injury. Following TAI, the IL-1-neutralizing antibody resulted in an improved behavioural outcome, including normalized behavioural profiles in the MCSF test. The performance in the MWM probe (memory) trial was improved, although not in the learning trials. The IL-1-neutralizing treatment did not influence cerebral ventricle size or the number of microglia/macrophages. These findings support the hypothesis that IL-1 is an important contributor to the processes causing complex cognitive and behavioural disturbances following TAI.
机译：广泛的创伤性轴索损伤（TAI）导致脑网络功能障碍，通常导致创伤性脑损伤（TBI）后持续的认知和行为障碍。 TBI引起复杂的神经炎症反应，通常位于轴突病理部位。 TAI中尚未确定促炎性细胞因子白介素（IL）-1的作用。 IL-1中和性抗体或对照抗体是在中心性液体敲击损伤（cFPI）（广泛的TAI的小鼠模型）后30分钟腹膜内给予的。将经受中度cFPI（n = 41）的小鼠与假手术的对照组（n = 20）和未经治疗的幼稚小鼠（n = 9）进行比较。在cFPI（n = 5）和假伤（n = 3）小鼠受伤后24小时，抗IL-1抗体均以适当的治疗浓度（高达30g /脑组织）到达靶脑区域，损伤后72h的浓度较低（三只cFPI小鼠的脑组织中最高可达18g / g）。在受伤后第2天和第9天使用多变量同心正方形场（MCSF）测试分析功能结果，在受伤后第14-21天用莫里斯水迷宫（MWM）分析功能结果。 TAI后，IL-1中和抗体可改善行为结果，包括MCSF测试中的行为规范化。 MWM探针（记忆）试验的性能得到了改善，尽管学习试验中没有。 IL-1中和治疗不会影响脑室大小或小胶质细胞/巨噬细胞的数量。这些发现支持以下假设：IL-1是导致TAI后引起复杂的认知和行为障碍的过程的重要贡献者。

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