Neurotransmitter release evoked by nerve impulses without Ca2+ entry through Ca2+ channels in frog motor nerve endings.
Neurotransmitter release evoked by nerve impulses without Ca2+ entry through Ca2+ channels in frog motor nerve endings.
复制标题
神经冲动引起的神经递质释放，无需通过青蛙运动神经末梢的 Ca2 通道进入。
DOI：
10.1113/jphysiol.1995.sp020536
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
MacDonald,RC
中科院分区：
文献类型：
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作者：
Silinsky,EM;Watanabe,M;Redman,RS;Qiu,R;Hirsh,JK;Hunt,JM;Solsona,CS;Alford,S;MacDonald,RC
1.在蛙骨骼肌终板上测定了神经冲动诱发乙酰胆碱（ACh）释放过程中对细胞外Ca ~（2+）的需求。在阻止Ca 2+从细胞外液进入的条件下，使用含Ca（2+）的脂质囊泡（Ca 2+脂质体）升高细胞质Ca 2+浓度。2.在不含Ca 2+和1 mM Mg 2+的细胞外溶液（“不含Ca（2+）”溶液）中，Ca 2+脂质体促进ACh量子的同步释放，在电生理学上反映为终板电位（EPP），响应于暂时隔离的神经冲动。3.运动神经刺激在用含Ca 2+通道阻断剂Co2+（1 mM）和Ca 2+螯合剂EGTA（2 mM）的无Ca（2+）溶液中的Ca 2+脂质体灌注期间产生了EPP。作为Ca ~（2+）从脂质体渗漏到细胞外液的生理对照，研究了Ca ~（2+）脂质体对由Ba ~（2+）介导的异步诱发ACh释放的影响。与0.2 - 0.3 mM细胞外Ca 2+产生EPP但拮抗Ba（2+）介导的异步ACh释放的作用相反，Ca 2+脂质体产生EPP但不减少Ba（2+）介导的异步释放。因此，Ca 2+脂质体的作用不是由于Ca 2+从脂质体泄漏到细胞外液。4.使用荧光标记的脂质体结合共聚焦显微镜的形态学研究表明，脂质从脂质体转移到神经末梢和脂质体内容物被递送到神经末梢细胞质。5.结果表明，当使用脂质体作为媒介物的细胞内Ca 2+升高时，诱发的ACh释放可以在没有Ca 2+通过Ca 2+通道进入的情况下发生。
1. The requirement for extracellular Ca2+ in the process of evoked acetylcholine (ACh) release by nerve impulses was tested at endplates in frog skeletal muscle. Ca(2+)‐containing lipid vesicles (Ca2+ liposomes) were used to elevate cytoplasmic Ca2+ concentrations under conditions in which Ca2+ entry from the extracellular fluid was prevented. 2. In an extracellular solution containing no added Ca2+ and 1 mM Mg2+ (‘Ca(2+)‐free’ solution), Ca2+ liposomes promoted the synchronous release of ACh quanta, reflected electrophysiologically as endplate potentials (EPPs), in response to temporally isolated nerve impulses. 3. Motor nerve stimulation generated EPPs during superfusion with Ca2+ liposomes in Ca(2+)‐free solutions containing the Ca2+ channel blocker Co2+ (1 mM), and the Ca2+ chelator EGTA (2 mM). As a physiological control for Ca2+ leakage from the liposomes to the extracellular fluid, the effect of Ca2+ liposomes on asynchronous evoked ACh release mediated by Ba2+ was examined. In contrast to the effects of 0.2‐0.3 mM extracellular Ca2+, which generated EPPs but antagonized Ba(2+)‐mediated asynchronous ACh release, Ca2+ liposomes generated EPPs but did not reduce asynchronous release mediated by Ba2+. The effects of Ca2+ liposomes were thus not due to leakage of Ca2+ from the liposome to the extracellular fluid. 4. Morphological studies using fluorescently labelled liposomes in conjunction with a confocal microscope demonstrate that lipid is transferred from the liposomes to nerve endings and liposomal contents are delivered to the nerve terminal cytoplasm. 5. The results suggest that when intracellular Ca2+ is elevated using liposomes as a vehicle, evoked ACh release can occur in the absence of Ca2+ entry via Ca2+ channels.