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Abstract：
OBJECTIVE: To assess the effects of repeated mild traumatic brain injury (rmTBI) in the parietal cortex on neuronal morphology and synaptic plasticity in the medulla oblongata of mice.
METHODS: Thirty-two male ICR mice were randomly divided into sham operation group (n=8) and rmTBI group (n=24). The mice in the latter group were subjected to repeated mild impact injury of the parietal cortex by a free-falling object. The mice surviving the injuries were evaluated for neurological deficits using neurological severity scores (NSS), righting reflex test and forced swimming test, and pathological changes of the neuronal cells in the medulla oblongata were observed with HE and Nissl staining. Western blotting and immunofluorescence staining were used to detect the expressions of neuroligin 1(NLG-1) and postsynaptic density protein 95(PSD-95) in the medulla oblongata of the mice that either survived rmTBI or not.
RESULTS: None of the mice in the sham-operated group died, while the mortality rate was 41.67% in rmTBI group. The mice surviving rmTBI showed significantly reduced NSS, delayed recovery of righting reflex, increased immobility time in forced swimming test (P < 0.05), and loss of Nissl bodies; swelling and necrosis were observed in a large number of neurons in the medulla oblongata, where the expression levels of NLG-1 and PSD-95 were significantly downregulated (P < 0.05). The mice that did not survive rmTBI showed distorted and swelling nerve fibers and decreased density of neurons in the medulla oblongina with lowered expression levels of NLG-1 and PSD-95 compared with the mice surviving the injuries (P < 0.01).
CONCLUSIONS: The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.
METHODS: Thirty-two male ICR mice were randomly divided into sham operation group (n=8) and rmTBI group (n=24). The mice in the latter group were subjected to repeated mild impact injury of the parietal cortex by a free-falling object. The mice surviving the injuries were evaluated for neurological deficits using neurological severity scores (NSS), righting reflex test and forced swimming test, and pathological changes of the neuronal cells in the medulla oblongata were observed with HE and Nissl staining. Western blotting and immunofluorescence staining were used to detect the expressions of neuroligin 1(NLG-1) and postsynaptic density protein 95(PSD-95) in the medulla oblongata of the mice that either survived rmTBI or not.
RESULTS: None of the mice in the sham-operated group died, while the mortality rate was 41.67% in rmTBI group. The mice surviving rmTBI showed significantly reduced NSS, delayed recovery of righting reflex, increased immobility time in forced swimming test (P < 0.05), and loss of Nissl bodies; swelling and necrosis were observed in a large number of neurons in the medulla oblongata, where the expression levels of NLG-1 and PSD-95 were significantly downregulated (P < 0.05). The mice that did not survive rmTBI showed distorted and swelling nerve fibers and decreased density of neurons in the medulla oblongina with lowered expression levels of NLG-1 and PSD-95 compared with the mice surviving the injuries (P < 0.01).
CONCLUSIONS: The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.
摘要：
目的：评估顶叶皮质反复轻度创伤性脑损伤（rmTBI）对小鼠延髓神经元形态和突触可塑性的影响。
方法：32只雄性ICR小鼠随机分为假手术组(n=8)和rmTBI组(n=24)。后一组中的小鼠受到自由落体对顶叶皮质的反复轻度冲击损伤。使用神经严重程度评分（NSS）评估存活的小鼠的神经功能缺损，扶正反射测试和强迫游泳测试，HE和Nissl染色观察延髓神经元细胞的病理变化。免疫印迹和免疫荧光染色检测神经凝集素1(NLG-1)和突触后密度蛋白95(PSD-95)在rmTBI存活或不存活小鼠延髓中的表达。
结果：假手术组小鼠均无死亡，rmTBI组死亡率为41.67%。存活的rmTBI小鼠显示NSS显著降低,扶正反射的延迟恢复，强迫游泳试验不动时间增加(P<0.05),和Nissl体的丢失；在延髓中的大量神经元中观察到肿胀和坏死，其中NLG-1和PSD-95的表达水平显著下调(P<0.05)。与未存活的小鼠相比，未存活的小鼠表现出神经纤维扭曲和肿胀，延髓中神经元密度降低，NLG-1和PSD-95的表达水平降低（P<0.01）。
结论：延髓突触的结构和功能异常可能导致小鼠rmTBI后的死亡和神经功能缺损。
方法：32只雄性ICR小鼠随机分为假手术组(n=8)和rmTBI组(n=24)。后一组中的小鼠受到自由落体对顶叶皮质的反复轻度冲击损伤。使用神经严重程度评分（NSS）评估存活的小鼠的神经功能缺损，扶正反射测试和强迫游泳测试，HE和Nissl染色观察延髓神经元细胞的病理变化。免疫印迹和免疫荧光染色检测神经凝集素1(NLG-1)和突触后密度蛋白95(PSD-95)在rmTBI存活或不存活小鼠延髓中的表达。
结果：假手术组小鼠均无死亡，rmTBI组死亡率为41.67%。存活的rmTBI小鼠显示NSS显著降低,扶正反射的延迟恢复，强迫游泳试验不动时间增加(P<0.05),和Nissl体的丢失；在延髓中的大量神经元中观察到肿胀和坏死，其中NLG-1和PSD-95的表达水平显著下调(P<0.05)。与未存活的小鼠相比，未存活的小鼠表现出神经纤维扭曲和肿胀，延髓中神经元密度降低，NLG-1和PSD-95的表达水平降低（P<0.01）。
结论：延髓突触的结构和功能异常可能导致小鼠rmTBI后的死亡和神经功能缺损。
