新疆医科大学学报
新疆醫科大學學報
신강의과대학학보
JOURNAL OF XINJIANG MEDICAL UNIVERSITY
2014年
8期
985-988
,共4页
于婵娟%刘亚华%田亮%黄春阳%刘涛%蒋晖
于嬋娟%劉亞華%田亮%黃春暘%劉濤%蔣暉
우선연%류아화%전량%황춘양%류도%장휘
海马 CA1 区%依托咪酯%兴奋性突触后电流%I-V 曲线%单通道氯电流
海馬 CA1 區%依託咪酯%興奮性突觸後電流%I-V 麯線%單通道氯電流
해마 CA1 구%의탁미지%흥강성돌촉후전류%I-V 곡선%단통도록전류
Hippocampal CA1 region%etomidate%excitatory postsynaptic currents%I-V curve%single channel chloride currents
目的:探讨静脉麻醉药物依托咪酯对大鼠海马 CA1区兴奋性突触后电流(excitatory postsynaptic cur-rents,EPSCs)的电流-电压(I-V)曲线在离子通道层面的影响机制。方法采用断头法分离 Wistar 大鼠海马脑半球,运用切片机制作400μm 厚度的海马脑部切片。切片分别置于60μL 脂肪乳剂和依托咪酯(相当于10μmol/L)乳剂中孵育40 min。在 Schaeffer 侧支/联合纤维处给予单个刺激,同时改变 CA1锥体神经元细胞膜钳制电位(-100~+40 mV 时,变化幅度为20 mV),绘制 I-V 曲线,并且采用膜片钳内面向外式记录技术全程记录外向整流特性的单通道氯电流。结果在保持膜钳制电位-70 mV 的条件下,10μmol/L 的依托咪酯降低反转电位,其电位由-53 mV 左右降低为-60 mV 左右,I-V 曲线左移,相应的单通道氯电流明显增强,通道开放程度增加。结论在静息状态下,依托咪酯主要作用于兴奋性突触后膜 GABAA 受体,通过使其 EPSCs 的离子构成发生变化抑制兴奋性突触活动,此过程中外向的电流分量增加,发生的主要改变可能为氯离子的跨膜转运。
目的:探討靜脈痳醉藥物依託咪酯對大鼠海馬 CA1區興奮性突觸後電流(excitatory postsynaptic cur-rents,EPSCs)的電流-電壓(I-V)麯線在離子通道層麵的影響機製。方法採用斷頭法分離 Wistar 大鼠海馬腦半毬,運用切片機製作400μm 厚度的海馬腦部切片。切片分彆置于60μL 脂肪乳劑和依託咪酯(相噹于10μmol/L)乳劑中孵育40 min。在 Schaeffer 側支/聯閤纖維處給予單箇刺激,同時改變 CA1錐體神經元細胞膜鉗製電位(-100~+40 mV 時,變化幅度為20 mV),繪製 I-V 麯線,併且採用膜片鉗內麵嚮外式記錄技術全程記錄外嚮整流特性的單通道氯電流。結果在保持膜鉗製電位-70 mV 的條件下,10μmol/L 的依託咪酯降低反轉電位,其電位由-53 mV 左右降低為-60 mV 左右,I-V 麯線左移,相應的單通道氯電流明顯增彊,通道開放程度增加。結論在靜息狀態下,依託咪酯主要作用于興奮性突觸後膜 GABAA 受體,通過使其 EPSCs 的離子構成髮生變化抑製興奮性突觸活動,此過程中外嚮的電流分量增加,髮生的主要改變可能為氯離子的跨膜轉運。
목적:탐토정맥마취약물의탁미지대대서해마 CA1구흥강성돌촉후전류(excitatory postsynaptic cur-rents,EPSCs)적전류-전압(I-V)곡선재리자통도층면적영향궤제。방법채용단두법분리 Wistar 대서해마뇌반구,운용절편궤제작400μm 후도적해마뇌부절편。절편분별치우60μL 지방유제화의탁미지(상당우10μmol/L)유제중부육40 min。재 Schaeffer 측지/연합섬유처급여단개자격,동시개변 CA1추체신경원세포막겸제전위(-100~+40 mV 시,변화폭도위20 mV),회제 I-V 곡선,병차채용막편겸내면향외식기록기술전정기록외향정류특성적단통도록전류。결과재보지막겸제전위-70 mV 적조건하,10μmol/L 적의탁미지강저반전전위,기전위유-53 mV 좌우강저위-60 mV 좌우,I-V 곡선좌이,상응적단통도록전류명현증강,통도개방정도증가。결론재정식상태하,의탁미지주요작용우흥강성돌촉후막 GABAA 수체,통과사기 EPSCs 적리자구성발생변화억제흥강성돌촉활동,차과정중외향적전류분량증가,발생적주요개변가능위록리자적과막전운。
Objective To observe the intravenous anesthetic etomidate on hippocampal CA1 excitatory postsynaptic currents (excitatory postsynaptic currents,EPSCs)current-voltage (I-V)curve in the level of ion channel mechanisms.Methods Decapitation wistar rat hippocampal hemispheres were separated by using slicing machine production 400 μm thickness hippocampal brain slices.Slices were placed in 60 μl fat emulsion or etomidate (equivalent to 10 μmol/L)of emulsions,and incubated for 40 minutes.In Schaeffer collateral/Allied Fiber was given a single stimulus,while changing the CA1 pyramidal neuron membrane holding potential (-100 mV to~+40 mV,the variation amplitude of 20 mV),drawing current-voltage (I-V)curve,and the use of membrane inside-out patch-clamp recording technique full record outwardly rectifying chloride current channel characteristics.Results Maintaining membrane potential of - 70 mV clamped condition,10 μmol/L reduced etomidate emulsion reversal potential,the electric potential of about -53 mV to -60 mV or so reduced,the I-V curve to the left,the corresponding channel chlorine current occurs significantly enhanced channel opening degree increases.Conclusion In the resting state, etomidate played a major role in the excitatory postsynaptic membrane GABAA receptors,ion composition by making changes EPSCs inhibition of excitatory synaptic activity,this process foreign to the current component increases,major changes may occur as transmembrane transport of Cl- .