中华神经外科杂志
中華神經外科雜誌
중화신경외과잡지
Chinese Journal of Neurosurgery
2012年
3期
299-303
,共5页
苗露%王峰%张雪峰%王恩杰%徐进%宋子木%孙涛
苗露%王峰%張雪峰%王恩傑%徐進%宋子木%孫濤
묘로%왕봉%장설봉%왕은걸%서진%송자목%손도
杏仁核%癫痫%活性调节细胞骨架蛋白%k252a%脑源性神经生长因子
杏仁覈%癲癇%活性調節細胞骨架蛋白%k252a%腦源性神經生長因子
행인핵%전간%활성조절세포골가단백%k252a%뇌원성신경생장인자
Amygadala%Epilepsy%Activity-regulated cytoskeletal protein%k252a%Brain-derived neurotrophic factor
目的 探讨BDNF - TrkB信号传导通路与杏仁核电刺激点燃大鼠Arc表达及癫痫发生的关系.方法 雄性SD大鼠随机分为空白组、假手术组、杏仁核点燃组(单纯点燃组、k252a注射组、DMSO对照组).应用Alpha - Lab 4通道信号采集及处理系统记录大鼠脑电活动.运用免疫组化检测其Arc蛋白的表达水平,采用RT - PCR、原位杂交检测Arc mRNA在海马中表达水平.结果 k252a注射组大鼠V级发作持续时间(33.00±1.41)8显著低于单纯点燃组(60.50±2.07)s、DMSO对照组(60.00±1.79)s大鼠V级发作持续时间(P<0.01).k252a注射组3h、6hArc阳性细胞百分率显著低于单纯点燃组、DMSO对照组3h、6hArc阳性细胞百分率(P<0.01),12 h时5组间Arc阳性细胞百分率相比表达差异无统计学意义(F =0.684,P>0.05).RT - PCR、原位杂交结果显示:k252a注射组1h、3 h Arc mRNA表达量显著低于单纯点燃组、DMSO对照组1h、3 h Arc mRNA表达量(P<0.01).6h时5组间Arc mRNA相比表达差异无统计学意义(P>0.05).结论 k252a能够抑制BDNF - TrkB 信号传导通路对Arc表达的诱导作用从而使癫痫发作的持续时间缩短.
目的 探討BDNF - TrkB信號傳導通路與杏仁覈電刺激點燃大鼠Arc錶達及癲癇髮生的關繫.方法 雄性SD大鼠隨機分為空白組、假手術組、杏仁覈點燃組(單純點燃組、k252a註射組、DMSO對照組).應用Alpha - Lab 4通道信號採集及處理繫統記錄大鼠腦電活動.運用免疫組化檢測其Arc蛋白的錶達水平,採用RT - PCR、原位雜交檢測Arc mRNA在海馬中錶達水平.結果 k252a註射組大鼠V級髮作持續時間(33.00±1.41)8顯著低于單純點燃組(60.50±2.07)s、DMSO對照組(60.00±1.79)s大鼠V級髮作持續時間(P<0.01).k252a註射組3h、6hArc暘性細胞百分率顯著低于單純點燃組、DMSO對照組3h、6hArc暘性細胞百分率(P<0.01),12 h時5組間Arc暘性細胞百分率相比錶達差異無統計學意義(F =0.684,P>0.05).RT - PCR、原位雜交結果顯示:k252a註射組1h、3 h Arc mRNA錶達量顯著低于單純點燃組、DMSO對照組1h、3 h Arc mRNA錶達量(P<0.01).6h時5組間Arc mRNA相比錶達差異無統計學意義(P>0.05).結論 k252a能夠抑製BDNF - TrkB 信號傳導通路對Arc錶達的誘導作用從而使癲癇髮作的持續時間縮短.
목적 탐토BDNF - TrkB신호전도통로여행인핵전자격점연대서Arc표체급전간발생적관계.방법 웅성SD대서수궤분위공백조、가수술조、행인핵점연조(단순점연조、k252a주사조、DMSO대조조).응용Alpha - Lab 4통도신호채집급처리계통기록대서뇌전활동.운용면역조화검측기Arc단백적표체수평,채용RT - PCR、원위잡교검측Arc mRNA재해마중표체수평.결과 k252a주사조대서V급발작지속시간(33.00±1.41)8현저저우단순점연조(60.50±2.07)s、DMSO대조조(60.00±1.79)s대서V급발작지속시간(P<0.01).k252a주사조3h、6hArc양성세포백분솔현저저우단순점연조、DMSO대조조3h、6hArc양성세포백분솔(P<0.01),12 h시5조간Arc양성세포백분솔상비표체차이무통계학의의(F =0.684,P>0.05).RT - PCR、원위잡교결과현시:k252a주사조1h、3 h Arc mRNA표체량현저저우단순점연조、DMSO대조조1h、3 h Arc mRNA표체량(P<0.01).6h시5조간Arc mRNA상비표체차이무통계학의의(P>0.05).결론 k252a능구억제BDNF - TrkB 신호전도통로대Arc표체적유도작용종이사전간발작적지속시간축단.
Objective To study the relationship of BDNF - TrkB signaling pathway and the expression of Arc in amygdala electrical stimulation kindled rats and the epilepsy.Methods Male SD rats were divided randomly into control group,sham group and amygdala kindled group (simple kindling group,k252a injection group,DMSO control group).Application of Alpha - Lab 4 channel signal acquisition and processing system recording the EEG activity of rats.The expression level of Arc gene in hippocampus was test by RT - PCR and hybridization,The expression level of Arc protein was test by immunohistochemistry.Results The V class insultus duration of k252a injection group rats (33.00 ± 1.41 )s,they were significantly less than the simple kindling group rats(60.50 ± 2.07) s and the DMSO control group rats(60.00 ± 1.79) s( P <0.01 ).The Arc of positive cells percentage was significantly lower at 3 h,6 h in k252a injection group than simple kinding group,DMSO control group( P < 0.01 ).The expression of Arc positive cells percentage among 5 groups at 12 h was no statistically significant ( F =0.684,P > 0.05 ).The resulted of RT - PCR,hybridization showing:The expression of Arc mRNA at 1 h,3 hsignificantly lower in k252a injection group than simple kinding group,DMSO control group( P < 0.01 )The defference of expression of Arc mRNA at 6 h among 5 groups was no statistically significant ( P >0.05 ).Conclusion k252a can inhibiting BDNF- TrkB signaling pathyway inducing the expression of Arc,to reduce the duration of seizure.