摘要
目的在氯化锂-匹鲁卡品诱发大鼠癫痫持续状态(SE)模型中探讨迷走神经刺激(VNS)对SE的影响。方法48只Wistar雄性大鼠按照随机数字表法分为4组:A组(VNS预处理组),注射匹鲁卡品前2h开始VNS刺激;B组(VNS治疗组),注射匹鲁卡品后开始VNS刺激;C组r阴性对照组),行VNS电极植入但不予刺激;D组(模型对照组),不予VNS电极植入;每组12只。采用氯化锂-匹鲁卡品腹腔注射诱发大鼠SE。VNS参数:频率30Hz,波宽500μs,电流1mA,刺激时间30S,间隔30S。观察各组大鼠行为学改变,72h后脑组织切片检测各组海马齿状回Caspase-3表达变化。结果(1)A、B组大鼠Ⅳ、Ⅴ级(Racine分级)发作次数明显少于C、D组,A组V级发作次数明显少于B组,A组sE潜伏期较其他各组均延长,差异均有统计学意义(P〈0.05)。(2)A、B2组大鼠海马齿状回Caspase-3表达量明显低于C、D2组似值分别为5854.7±856.5、6244.8±806.0;11957.0±1948.1、11543.2±1734.7),差异有统计学意义衅0.05)。结论VNS能够使SE大鼠行为学得到改善。且VNS预处理效果优于治疗性VNS刺激;VNS能够减少SE导致的海马神经元早期凋亡,对海马神经元有保护作用。
Objective To study the acute effect of vagus nerve stimulation (VNS) on status epileptieus (SE) in rats. Methods Forty-eight male Wistar rats were randomly divided into 4 groups: Group A (VNS preconditioning group), accepted VNS at 2 h before pilocarpine injection, Group B (VNS treatment group), accepted VNS immediately after pilocarpine injection, Group C (negative control group), implanted with electrode without stimulation, and Group D (SE model group), without electrode implantation (n=12). Lithium-pilocarpine was used to kindle the rats to establish SE models. Stimulation parameters used in the procedure of VNS were as follows: frequency, 30 Hz; pulse width, 0.5 ms; current, 1 mA; and duty cycle, on-30 s, off-30 s. Behavior changes were observed and caspase-3 expression in dentate gyrus was detected 72 h after pilocarpine injection. Results (1) The seizure frequencies of grade 1V and V (Racine grading) in group A and B were significantly fewer than those in group C and D (P〈0.05); the seizure frequency of grade V in group A was significantly fewer than that of group B (P〈0.05); SE latency in group A was significantly longer than that in other groups (P〈0.05). (2) Expressions of caspase-3 in the dentate gyms of group A and B were significantly lower than those of group C and D (absorbancy values being 5854.7±856.5, 6244.8±806.0, 11957.0±1948.1 and 11543.2±1734.7,P〈0.05). Conclusion VNS has an acute seizure-suppressing effect on SE in rats and it can also reduce neuronal apoptosis induced by SE in hipocampus.
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2014年第11期1097-1100,共4页
Chinese Journal of Neuromedicine