Calcium currents at motor nerve endings: absence of effects of adenosine receptor agonists in the frog.
Calcium currents at motor nerve endings: absence of effects of adenosine receptor agonists in the frog.
复制标题
运动神经末梢的钙电流：青蛙中缺乏腺苷受体激动剂的作用。
DOI：
10.1113/jphysiol.1992.sp019380
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Solsona,CS
中科院分区：
文献类型：
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作者：
Silinsky,EM;Solsona,CS
1. 研究了腺苷（50 μ m）和2‐氯腺苷（1‐25 μ m）对蛙运动神经末梢Ca2+电流的影响。2. 与同步相关的Ca2+电流，神经诱发释放乙酰胆碱（ACh）使用神经周围或贴片记录方法进行测量。四乙基铵和/或3,4 -二氨基吡啶被用来阻断K+电流。3. omega‐concontoxin（1.5‐2.5 microM）、Cd2+ （100 microM‐2 mM）、Co2+ （500 microM‐5 mM）或细胞外钙浓度的降低可抑制Ca2+电流。当Sr2+取代Ca2+时，也观察到这种电流。据报道，在该物种中，运动神经末梢的ACh释放和Ca2+电流对1,4‐二氢吡啶拮抗剂不敏感。4. 腺苷受体激动剂在产生最大抑制乙酰胆碱释放的浓度下不影响Ca2+电流。5. 在Ca2+浓度梯度可能逆转的条件下（含有1mm EGTA的无Ca(2+) Ringer溶液），腺苷受体激动剂对异步K（+）依赖性ACh释放的影响进行了研究。通过监测微终板电位（MEPPs）的发生频率来测定乙酰胆碱释放。在含有1mm EGTA的无Ca（2+）溶液中，高K+去极化导致MEPP频率降低，可能是因为它引起Ca2+从神经末梢通过膜Ca2+通道以反向Ca2+梯度流出。6. Ca2+通道阻滞剂Co2+，阻断Ca2+从神经末梢的出口，以浓度依赖的方式增加MEPPs的频率在反向Ca2+梯度。7. 腺苷或2 -氯腺苷在反向Ca2+梯度中抑制乙酰胆碱释放。8. 结果表明，Ca2+进入的阻断不是腺苷对蛙运动神经末梢的抑制作用的原因。
1. The effects of adenosine (50 microM) and 2‐chloroadenosine (1‐25 microM) were studied on Ca2+ currents in frog motor nerve endings. 2. Ca2+ currents associated with the synchronous, neurally evoked release of acetylcholine (ACh) were measured using either perineural or patch recording methods. Tetraethylammonium and/or 3,4‐diaminopyridine were employed to block K+ currents. 3. Ca2+ currents were depressed by omega‐conotoxin (1.5‐2.5 microM), Cd2+ (100 microM‐2 mM), Co2+ (500 microM‐5 mM) or by a reduction of the extracellular calcium concentration. Such currents were also observed when Sr2+ was substituted for Ca2+. Both ACh release and Ca2+ currents at motor nerve endings have been reported to be insensitive to 1,4‐dihydropyridine antagonists in this species. 4. Adenosine receptor agonists did not affect Ca2+ currents at concentrations that produced maximal inhibition of ACh release. 5. The effects of adenosine receptor agonists were examined on asynchronous K(+)‐dependent ACh release under conditions in which the Ca2+ concentration gradient is likely to be reversed (Ca(2+)‐free Ringer solution containing 1 mM EGTA). ACh release was measured by monitoring the frequency of occurrence of miniature endplate potentials (MEPPs). In Ca(2+)‐free solutions containing 1 mM EGTA, high K+ depolarization caused a decrease in MEPP frequency, presumably because it elicits the efflux of Ca2+ from the nerve ending via membrane Ca2+ channels in a reverse Ca2+ gradient. 6. The Ca2+ channel blocker Co2+, which blocks the exit of Ca2+ from the nerve ending, increased the frequency of MEPPs in a concentration‐dependent manner in a reverse Ca2+ gradient. 7. Adenosine or 2‐chloroadenosine inhibited ACh release in a reverse Ca2+ gradient. 8. The results suggest that blockade of Ca2+ entry is not responsible for the inhibitory effects of adenosine at frog motor nerve endings.