Li M, He L, Li T, Bao Y, Xu X, Chen G
School of Forensic Medicine, Wannan Medical College, Wuhu 241000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 May 20;44(5):960-966. doi: 10.12122/j.issn.1673-4254.2024.05.18.
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.
Thirty-two male ICR mice were randomly divided into sham operation group (=8) and rmTBI group (=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.
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 ( < 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 ( < 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 ( < 0.01).
The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.
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。
将32只雄性ICR小鼠随机分为假手术组(n = 8)和rmTBI组(n = 24)。后者通过自由落体物体对顶叶皮质进行反复轻度撞击损伤。对受伤后存活的小鼠使用神经严重程度评分(NSS)、翻正反射试验和强迫游泳试验评估神经功能缺损,并通过苏木精-伊红(HE)染色和尼氏染色观察延髓神经元细胞的病理变化。采用蛋白质免疫印迹法和免疫荧光染色法检测rmTBI存活或未存活小鼠延髓中神经连接蛋白1(NLG-1)和突触后致密蛋白95(PSD-95)的表达。
假手术组小鼠均未死亡,而rmTBI组死亡率为41.67%。rmTBI存活小鼠的NSS显著降低,翻正反射恢复延迟,强迫游泳试验中不动时间增加(P < 0.05),尼氏体丢失;延髓中大量神经元出现肿胀和坏死,其中NLG-1和PSD-95的表达水平显著下调(P < 0.05)。与受伤存活小鼠相比,rmTBI未存活小鼠的神经纤维扭曲肿胀,延髓中神经元密度降低,NLG-1和PSD-95表达水平降低(P < 0.01)。
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损害。