低频经颅磁刺激对匹罗卡品致痫大鼠癫痫发作及海马细胞神经肽Y表达的影响

Low frequency transcranial magnetic stimulation changes seizure and neuropeptide Y expression of hippocampal neurons in rats epilepsy induced by pilocarpine

目的观察低频经颅磁刺激(LF-TMS)对匹罗卡品(PLO)致痫大鼠皮质脑电图及大鼠海马各区神经肽Y(NPY)表达的影响。方法雄性SD大鼠40只,随机分为对照组(PLO组)、干预组(PLO+LF- TMS组)。各组给予相关干预处理后腹腔注射PLO建立癫痫模型,观察皮质脑电图及海马HE染色、NPY免疫组化染色观察。结果两组间皮质脑电图指标比较,发现磁刺激干预后潜伏期延长、痫波频率及大发作次数降低。HE染色显示,对照组海马各区神经元显著变性、死亡,以海马CA3区明显;干预组海马各区神经元损害减轻。NPY的免疫组化染色显示对照组各时间点海马各区NPY阳性细胞增多,明显高于干预组,差异有统计学意义。结论LF-TMS不仅可以延迟PLO癫痫点燃的形成,还可以缓解点燃后的癫痫发作程度;LF-TMS可明显影响海马各区NPY阳性细胞数。NPY与癫痫发作程度相关,提示NPY表达与癫痫之间关系紧密,NPY可能具有抗痫和神经保护作用。

Objective To observe the effects of low frequency transcranial magnetic stimulation （LF-TMS） on the electroencephalogram （EEG） , expression of NPY in hippocampus in pilocarpine （PLO） -induced epileptic rats. Methods Forty male Sprague-Dawley rats （240-260 g） were used to establish a model of epilepsy by intradominal injection of pilocarpine, and then randomized into 2 groups： a control group and an intervention group. The control group was treated by sham LF-TMS, while the intervention group was treated by LF-TMS once daily for 7 days. I group simply celiac inject pilocarpine. Ⅱ group celiac inject PLO after LF-TMS. The EEG was recorded in both groups and the checked pathology. Pathological item include HE staining, NPY immunohisto chemical staining. Results The latency for seizure attack was significantly lengthened, while the frequency of seizure attack and times of major seizure attack were significantly decreased in the intervention group. The HE staining revealed significant degeneration and necrosis of neurons in the hippocampus, especially in the CA3 region, in rats in the control group. The pathologic changes were significantly less severe in the intervention. Immunohistochemical staining showed a significantly higher expression of NPY in the hippocampus as compared with the intervention group. Conclusion Using the PLO-induced epilepsy model, LF-TMS could not only postpone the generation of kindling but also inhibit the progress of epilepsy. The increased NPY expression in the hippocampusin the intervention group implied a close rela- tionship between NPY and epilepsy attack.