重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
18期
2319-2322
,共4页
高轩%黄金伟%刘舒%李永秋%李洪亮%李莉萍
高軒%黃金偉%劉舒%李永鞦%李洪亮%李莉萍
고헌%황금위%류서%리영추%리홍량%리리평
低温%癫痫%γ氨基丁酸
低溫%癲癇%γ氨基丁痠
저온%전간%γ안기정산
hypothermia%epilepsy%gama-aminobutyric-acid
目的:观察低温在治疗癫痫发生过程中的细胞学机制。方法使用单-双-膜片钳技术,对4-氨基吡啶诱导的癫痫小鼠模型的海马和皮层神经元细胞进行穿孔,分别记录不同温度下细胞的电生理变化。结果持续低温能阻断4-氨基吡啶诱导的海马神经元的持续性放电并增加输入电阻。通过双-膜片钳记录显示相距较远的 CA1和 CA3区域的锥体神经元有显著的同步性,但锥体神经元和中间神经元间的同步性较弱。在CA1和CA3神经元中,低温可以阻断节律性动作电位的放电行为,并能破坏其同步性;但在中间神经元中低温阻断节律性放电时并不会破坏动作电位。结论低温对γ-氨基丁酸传导和分泌影响程度不同,干扰了神经网络的同步放电,从而阻断癫痫样放电。另外,γ-氨基丁酸释放导致的中间神经元动作电位持续放电,也增强了低温的抗癫痫作用。
目的:觀察低溫在治療癲癇髮生過程中的細胞學機製。方法使用單-雙-膜片鉗技術,對4-氨基吡啶誘導的癲癇小鼠模型的海馬和皮層神經元細胞進行穿孔,分彆記錄不同溫度下細胞的電生理變化。結果持續低溫能阻斷4-氨基吡啶誘導的海馬神經元的持續性放電併增加輸入電阻。通過雙-膜片鉗記錄顯示相距較遠的 CA1和 CA3區域的錐體神經元有顯著的同步性,但錐體神經元和中間神經元間的同步性較弱。在CA1和CA3神經元中,低溫可以阻斷節律性動作電位的放電行為,併能破壞其同步性;但在中間神經元中低溫阻斷節律性放電時併不會破壞動作電位。結論低溫對γ-氨基丁痠傳導和分泌影響程度不同,榦擾瞭神經網絡的同步放電,從而阻斷癲癇樣放電。另外,γ-氨基丁痠釋放導緻的中間神經元動作電位持續放電,也增彊瞭低溫的抗癲癇作用。
목적:관찰저온재치료전간발생과정중적세포학궤제。방법사용단-쌍-막편겸기술,대4-안기필정유도적전간소서모형적해마화피층신경원세포진행천공,분별기록불동온도하세포적전생리변화。결과지속저온능조단4-안기필정유도적해마신경원적지속성방전병증가수입전조。통과쌍-막편겸기록현시상거교원적 CA1화 CA3구역적추체신경원유현저적동보성,단추체신경원화중간신경원간적동보성교약。재CA1화CA3신경원중,저온가이조단절률성동작전위적방전행위,병능파배기동보성;단재중간신경원중저온조단절률성방전시병불회파배동작전위。결론저온대γ-안기정산전도화분비영향정도불동,간우료신경망락적동보방전,종이조단전간양방전。령외,γ-안기정산석방도치적중간신경원동작전위지속방전,야증강료저온적항전간작용。
Objective To investigate the cytological mechanism of the low temperature for treating the epilepsy occurrence process.Methods The hippocampus and cortex neurons in the 4-aminopyridine induced mouse epilepsy model were performed the perforation by using the single-and dual-patch clamp technique and the electrophysiologic changes under different temperatures were recorded respectively.Results The continuous low temperature could block the continuous discharge of the hippocampus neurons induced by 4-aminopyridine and increase the input resistance.The dual-patch clamp recordings showed that the pyramidal neurons in the CA1 and CA3 regions far apart from each other had the significant synchronism,but the synchronism between the pyramidal neurons and interneurons was weaker.In CA1 and CA3 neurons,hypothermia could block the rhythmic action potential discharges and destroyed their synchronism;however,in blocking rhythmic discharges of interneurons,hypothermia did not destroy the action potentials.Conclusion Hypothermia affects theγ-aminobutyric acid conduction and secretion to different degrees and interferes the synchronic discharge of neural network,thus blocks the epileptiform discharge.In addition,continuous discharge of interneurons ac-tion potentials induced byγ-aminobutyric acid release would enhance the antiepileptic effects of hypothermia.