Xue Shuaishuai, Yi Peiyao, Mao Yangqi, Zhan Zhengming, Cai Yonghua, Song Zibin, Wang Kewan, Yang Kaijun, Song Ye, Wang Xingqin, Long Hao
Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital of Southern Medical University, Guangzhou, China.
Epileptic Disord. 2025 Apr;27(2):204-218. doi: 10.1002/epd2.20316. Epub 2024 Nov 21.
Temporal lobe epilepsy (TLE) is the most prevalent form of epilepsy. Prior research has indicated the involvement of the nucleus accumbens shell (NAcSh) in the process of epileptogenesis, thereby implying its potential as a therapeutic target for TLE. In the present study, we investigated the antiepileptic effect of the NAcSh electrical lesion.
Chronic TLE was induced by stereotactic injection of kainic acid (KA) into the hippocampus 3 weeks after KA administration, and NAcSh electrical lesions were performed. Seizures in rats were monitored by video electroencephalogram (EEG) 1 week following the NAcSh electrical lesion. Besides, the spatial memory function assessment in rats was conducted using the Morris water maze (MWM) test in the final week of the experiment. Later, hippocampal glial cell activation and neuron loss in rats were evaluated through immunohistochemistry.
TLE rats subjected to NAcSh electrical lesion exhibited a significant reduction in the frequency of seizures compared to untreated TLE rats. Furthermore, NAcSh electrical lesion led to less activation of hippocampal glial cells and fewer neuronal loss in TLE rats. It is worth noting that the NAcSh electrical lesion did not cause additional memory impairment.
In the present study, the NAcSh electrical lesion exhibited a definitive therapeutic effect on the chronic TLE rat model, potentially due to decreased hippocampal TLE-induced activation of glial cells and neuron loss. In conclusion, our results indicated that the NAcSh is a promising therapeutic target for TLE and possesses high potential for clinical application.
颞叶癫痫（TLE）是最常见的癫痫形式。先前的研究表明伏隔核壳（NAcSh）参与癫痫发生过程，这意味着它有可能成为TLE的治疗靶点。在本研究中，我们研究了NAcSh电损伤的抗癫痫作用。
在给予 kainic 酸（KA）3周后，通过立体定向向海马注射KA诱导慢性TLE，并进行NAcSh电损伤。在NAcSh电损伤后1周，通过视频脑电图（EEG）监测大鼠的癫痫发作情况。此外，在实验的最后一周，使用莫里斯水迷宫（MWM）试验对大鼠的空间记忆功能进行评估。随后，通过免疫组织化学评估大鼠海马神经胶质细胞活化和神经元丢失情况。
与未治疗的TLE大鼠相比，接受NAcSh电损伤的TLE大鼠癫痫发作频率显著降低。此外，NAcSh电损伤导致TLE大鼠海马神经胶质细胞活化减少，神经元丢失减少。值得注意的是，NAcSh电损伤并未导致额外的记忆损害。
在本研究中，NAcSh电损伤对慢性TLE大鼠模型显示出明确的治疗效果，这可能是由于海马中TLE诱导的神经胶质细胞活化和神经元丢失减少。总之，我们的结果表明NAcSh是TLE的一个有前景的治疗靶点，具有很高的临床应用潜力。
