中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2014年
8期
542-547
,共6页
伍国锋%刘晓英%洪震%唐太峰
伍國鋒%劉曉英%洪震%唐太峰
오국봉%류효영%홍진%당태봉
癫痫,颞叶%抗药性,多药%海马%电刺激%细胞外液%γ氨基丁酸%杏仁核
癲癇,顳葉%抗藥性,多藥%海馬%電刺激%細胞外液%γ氨基丁痠%杏仁覈
전간,섭협%항약성,다약%해마%전자격%세포외액%γ안기정산%행인핵
Epilepsy,temporal lobe%Drug resistance,multiple drug%Hippocampus%Electric stimulation%Extracellular fluid%gamma-Aminobutyric acid%Amygdala
目的 建立多药耐药性颞叶癫痫模型,以杏仁核后放电频率、癫痫发作频率、海马细胞外液γ-氨基丁酸(GABA)浓度为指标,观察海马电刺激治疗耐药性颞叶癫痫的疗效及可能机制.方法 选用Wistar大鼠120只,制作慢性杏仁核点燃癫痫模型,模型制作成功后,应用经典抗癫痫药苯妥英钠和苯巴比妥进行筛选,根据癫痫大鼠对药物的反应区别出耐药性癫痫大鼠及药物敏感大鼠,将耐药性癫痫大鼠分为耐药对照组(n=8)及海马刺激组(n=8),对耐药性癫痫大鼠进行低频海马电刺激,用微透析方法收集脑组织细胞外液,采用高效液相色谱法检测海马电刺激后GABA含量的变化.结果 海马刺激组经过2周的低频电刺激后,癫痫发作受到明显抑制,杏仁核后放电频率及波幅降低,8:00-9:00 am和8:00-9:00 pm 2个时段的GABA浓度(μg/ml)分别为32.69±7.80、35.76±6.27,2个时段的GABA浓度(μg/ml)都明显高于耐药对照组(26.58±6.87,t=-21.45,P=0.000;31.50 ±4.87,t=-15.74,P=0.000),差异具有统计学意义.结论 低频电刺激海马可以明显抑制点燃模型的癫痫发作,抑制耐药性颞叶癫痫模型的后放电,降低杏仁核后放电频率及波幅、缩短后放电持续时间,该作用可能是通过增加脑细胞外液GABA浓度而实现的.
目的 建立多藥耐藥性顳葉癲癇模型,以杏仁覈後放電頻率、癲癇髮作頻率、海馬細胞外液γ-氨基丁痠(GABA)濃度為指標,觀察海馬電刺激治療耐藥性顳葉癲癇的療效及可能機製.方法 選用Wistar大鼠120隻,製作慢性杏仁覈點燃癲癇模型,模型製作成功後,應用經典抗癲癇藥苯妥英鈉和苯巴比妥進行篩選,根據癲癇大鼠對藥物的反應區彆齣耐藥性癲癇大鼠及藥物敏感大鼠,將耐藥性癲癇大鼠分為耐藥對照組(n=8)及海馬刺激組(n=8),對耐藥性癲癇大鼠進行低頻海馬電刺激,用微透析方法收集腦組織細胞外液,採用高效液相色譜法檢測海馬電刺激後GABA含量的變化.結果 海馬刺激組經過2週的低頻電刺激後,癲癇髮作受到明顯抑製,杏仁覈後放電頻率及波幅降低,8:00-9:00 am和8:00-9:00 pm 2箇時段的GABA濃度(μg/ml)分彆為32.69±7.80、35.76±6.27,2箇時段的GABA濃度(μg/ml)都明顯高于耐藥對照組(26.58±6.87,t=-21.45,P=0.000;31.50 ±4.87,t=-15.74,P=0.000),差異具有統計學意義.結論 低頻電刺激海馬可以明顯抑製點燃模型的癲癇髮作,抑製耐藥性顳葉癲癇模型的後放電,降低杏仁覈後放電頻率及波幅、縮短後放電持續時間,該作用可能是通過增加腦細胞外液GABA濃度而實現的.
목적 건립다약내약성섭협전간모형,이행인핵후방전빈솔、전간발작빈솔、해마세포외액γ-안기정산(GABA)농도위지표,관찰해마전자격치료내약성섭협전간적료효급가능궤제.방법 선용Wistar대서120지,제작만성행인핵점연전간모형,모형제작성공후,응용경전항전간약분타영납화분파비타진행사선,근거전간대서대약물적반응구별출내약성전간대서급약물민감대서,장내약성전간대서분위내약대조조(n=8)급해마자격조(n=8),대내약성전간대서진행저빈해마전자격,용미투석방법수집뇌조직세포외액,채용고효액상색보법검측해마전자격후GABA함량적변화.결과 해마자격조경과2주적저빈전자격후,전간발작수도명현억제,행인핵후방전빈솔급파폭강저,8:00-9:00 am화8:00-9:00 pm 2개시단적GABA농도(μg/ml)분별위32.69±7.80、35.76±6.27,2개시단적GABA농도(μg/ml)도명현고우내약대조조(26.58±6.87,t=-21.45,P=0.000;31.50 ±4.87,t=-15.74,P=0.000),차이구유통계학의의.결론 저빈전자격해마가이명현억제점연모형적전간발작,억제내약성섭협전간모형적후방전,강저행인핵후방전빈솔급파폭、축단후방전지속시간,해작용가능시통과증가뇌세포외액GABA농도이실현적.
Objective To establish a multi-drug resistant model of temporal lobe epilepsy and observe the effect of hippocampal stimulation on pharmacoresistant epileptic rats and its possible mechanism with the use of indexes including after discharges (AD) of the amygdalae,the stimulus-induced seizures and the extracellular levels of γ-aminobutyrate (GABA).Methods Totally,120 Wistar rats were used for the amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.Based on the successful kindled model of epilepsy,we selected the pharmacoresistant and pharmacosensitive epileptic rats according to their response to phenobabital and phenytoin.We then divided the pharmacoresistant epileptic rats into the hippocampal stimulation group and control group,with 8 rats in each group.Low-frequency stimulus was conducted for two weeks in the hippocampal stimulation group.The hippocampus extracellular fluid collected by microdialysis was then used to determine the levels of GABA by a high performance liquid chromatography method after hippocampal stimulation.Results The stimulus-induced seizures were inhibited significantly,and the frequency of the AD was decreased,as well as the amplitude,compared with the control group.The extracellular level of GABA in the 8:00-9:00 am and the 8:00-9:00 pm was (32.69 ± 7.80) and (35.76 ± 6.27) μg/ml,respectively,both significantly increased as compared with the control ((26.58 ± 6.87) μg/ml,t =-21.45,P =0.000 ; (31.50 ± 4.87) μg/ml,t =-15.74,P =0.000).Conclusions The low-frequency hippocampal stimulation inhibits the seizures of the kindled model of epilepsy and decreases the frequency,the amplitude,as well as the duration of the amygdale AD in the pharmacoresistant epileptic rats,which may be contributed to the increased GABA content in extracellular fluid of the brain after stimulation.
