INTRODUCTION To explore the effect of accumbens nucleus shell (ACbSh) lesioning on bitemporal lobe epilepsy. MATERIAL AND METHODS Adult Wistar rats (male) were enrolled and randomly assigned into the control group and epilepsy groups with multiple time-points. Lithium-pilocarpine was used to establish the rat epilepsy model, while the control group received an equal amount of saline. Ibotenic acid stereotaxic injection was performed to cause accumbens nucleus shell lesioning for specific groups. Cascade software was used for electroencephalogram (EEG) examination. Fluoro-Jade C staining was performed to examine neuronal degeneration. RESULTS Latency period of the epilepsy in epilepsy groups was 15.3 ± 1.1 min, and epilepsy intensity was 4.8 ± 0.5 events/ 12 h. ACbSh lesioning significantly reduced aggressive behavior. Compared with epilepsy groups without ACbSh lesioning, ACbSh lesioning significantly decreased epileptic seizures and reduced epileptic duration (p < 0.05). EEG showed that there were still sharp waves in the hippocampus and amygdala region after ACbSh lesioning, but epileptic discharge in prefrontal cortex was significantly decreased (p < 0.05), while epilepsy groups without ACbSh lesioning had more sharp waves in the prefrontal cortex, hippocampus and amygdala region. Fluoro-Jade C staining showed that ACbSh lesioning significantly decreased grades of neuronal degeneration (p < 0.05). CONCLUSIONS Recurrent epilepsy caused neuronal degeneration via ACbSh region-related pathways, and ACbSh lesioning could mitigate epilepsy-caused neuronal degeneration by reducing epileptic discharge.

中文翻译：

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大鼠伏隔核壳损伤对大鼠颞叶癫痫的影响。

引言探讨伏隔核壳（ACbSh）损伤对颞叶癫痫的影响。材料与方法纳入成年Wistar大鼠（雄性）并随机分为多个时间点的对照组和癫痫组。锂-毛果芸香碱用于建立大鼠癫痫模型，而对照组则接受等量的生理盐水。进行异麦芽酮酸立体定向注射以引起特定组的伏隔核壳损伤。级联软件用于脑电图（EEG）检查。进行荧光玉石C染色以检查神经元变性。结果癫痫组的癫痫潜伏期为15.3±1.1min，癫痫发作强度为4.8±0.5事件/ 12h。ACbSh损伤明显减少了攻击行为。与没有ACbSh损伤的癫痫组相比，ACbSh损伤显着减少了癫痫发作并缩短了癫痫持续时间（p <0.05）。脑电图显示ACbSh损伤后海马和杏仁核区域仍存在尖锐波，但额叶前皮层的癫痫放电显着减少（p <0.05），而未ACbSh损伤的癫痫组在前额皮层，海马和皮层有更多尖锐波。杏仁核地区。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。ACbSh损伤显着减少了癫痫发作并缩短了癫痫持续时间（p <0.05）。脑电图显示ACbSh损伤后海马和杏仁核区域仍存在尖锐波，但额叶前皮层的癫痫放电显着减少（p <0.05），而未ACbSh损伤的癫痫组在前额皮层，海马和皮层有更多尖锐波。杏仁核地区。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。ACbSh损伤显着减少了癫痫发作并缩短了癫痫持续时间（p <0.05）。脑电图显示ACbSh损伤后海马和杏仁核区域仍存在尖锐波，但额叶前皮层的癫痫放电显着减少（p <0.05），而未ACbSh损伤的癫痫组在前额皮层，海马和皮层有更多尖锐波。杏仁核地区。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。脑电图显示ACbSh损伤后海马和杏仁核区域仍存在尖锐波，但额叶前皮层的癫痫放电显着减少（p <0.05），而未ACbSh损伤的癫痫组在前额皮层，海马和皮层有更多尖锐波。杏仁核地区。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。脑电图显示ACbSh损伤后海马和杏仁核区域仍存在尖锐波，但额叶前皮层的癫痫放电显着减少（p <0.05），而未ACbSh损伤的癫痫组在前额皮层，海马和皮层有更多尖锐波。杏仁核地区。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。而没有ACbSh损伤的癫痫组在前额叶皮层，海马区和杏仁核区则有更多尖锐的波。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。而没有ACbSh损伤的癫痫组在前额叶皮层，海马区和杏仁核区则有更多尖锐的波。Fluoro-Jade C染色显示ACbSh损伤显着降低了神经元变性的等级（p <0.05）。结论复发性癫痫通过ACbSh区域相关途径引起神经元变性，而ACbSh病灶可通过减少癫痫放电减轻癫痫引起的神经元变性。