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海马神经发生在 LiCl-匹罗卡品诱导癫痫大鼠 ANT-DBS 中的作用。

The Role of Hippocampal Neurogenesis in ANT-DBS for LiCl-Pilocarpine-Induced Epileptic Rats.

机构信息

Department of Neurology, Xiangya Hospital, Central South University, Changsha, China.

Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China,

出版信息

Stereotact Funct Neurosurg. 2021;99(1):55-64. doi: 10.1159/000509314. Epub 2020 Dec 10.

DOI:10.1159/000509314
PMID:33302280
Abstract

PURPOSE

Abnormal neurogenesis in the hippocampus after status epilepticus (SE) has been suggested as a key pathogeny of temporal lobe epilepsy. This study aimed to investigate the effect of deep brain stimulation of the anterior thalamic nucleus (ANT-DBS) on hippocampal neurogenesis in LiCl-pilocarpine-induced epileptic rats and to analyze its relationship with postoperative spontaneous recurrent seizures (SRS) and anxiety.

METHOD

SE was induced by a systemic LiCl-pilocarpine injection in adult male rats. Rats in the DBS group underwent ANT-DBS immediately after successful SE induction. SRS was only recorded during the chronic stage. An elevated plus maze was used to evaluate the level of anxiety in rats 7, 28, and 60 days after SE onset. After the elevated plus-maze experiment, rats were sacrificed under anesthesia in order to evaluate hippocampal neurogenesis. Doublecortin (DCX) was used as a marker for neurogenesis.

RESULTS

During the chronic stage, SRS in rats in the DBS group were significantly decreased. The level of anxiety was increased significantly in rats in the DBS group 28 days after SE, while no significant differences in anxiety levels were found 7 and 60 days after SE. The number of DCX-positive cells in the hippocampus was significantly increased 7 days after SE and was significantly decreased 60 days after SE in all rats in which SE was induced. However, the number of DCX-positive cells in the DBS group was significantly lower than that in the other groups 28 days after SE.

CONCLUSIONS

ANT-DBS may suppress SRS and increase the postoperative anxiety of epileptic rats by influencing hippocampal neurogenesis.

摘要

目的

癫痫持续状态(SE)后海马体异常神经发生被认为是颞叶癫痫的关键发病机制。本研究旨在探讨前丘脑核深部脑刺激(ANT-DBS)对氯化锂-匹罗卡品诱导的癫痫大鼠海马神经发生的影响,并分析其与术后自发性复发癫痫(SRS)和焦虑的关系。

方法

通过给成年雄性大鼠腹腔注射氯化锂-匹罗卡品诱导 SE。DBS 组大鼠在 SE 成功诱导后立即进行 ANT-DBS。仅在慢性期记录 SRS。高架十字迷宫用于评估 SE 发作后 7、28 和 60 天大鼠的焦虑水平。高架十字迷宫实验后,大鼠在麻醉下处死,以评估海马神经发生。双皮质素(DCX)被用作神经发生的标志物。

结果

在慢性期,DBS 组大鼠的 SRS 明显减少。DBS 组大鼠在 SE 后 28 天的焦虑水平显著升高,而在 SE 后 7 和 60 天,焦虑水平无显著差异。SE 诱导后所有大鼠的海马体中 DCX 阳性细胞数量在 SE 后 7 天显著增加,在 SE 后 60 天显著减少。然而,DBS 组大鼠的 DCX 阳性细胞数量在 SE 后 28 天明显低于其他组。

结论

ANT-DBS 可能通过影响海马神经发生来抑制 SRS 和增加癫痫大鼠术后焦虑。

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