The effect of reduced temperature on the inhibitory action of adenosine and magnesium ion at frog motor nerve terminals.
The effect of reduced temperature on the inhibitory action of adenosine and magnesium ion at frog motor nerve terminals.
复制标题
降低温度对腺苷和镁离子对青蛙运动神经末梢抑制作用的影响。
DOI：
10.1111/j.1476-5381.1988.tb11470.x
复制
发表时间：
1988
影响因子：
7.3
通讯作者：
Hirsh,JK
中科院分区：
文献类型：
--
作者：
Silinsky,EM;Hirsh,JK
1进行了一项研究，以排除腺苷受体激动剂对去极化-分泌过程产生直接物理阻断的概念。降低温度被用作区分腺苷作用中的物理化学过程（例如介导诱发递质释放的过程）和生化机制（例如涉及第二信使物质的机制）的工具。腺苷和2-氯腺苷被用作从青蛙运动神经末梢释放乙酰胆碱（ACh）的电生理研究中的激动剂。2通过将制剂保持在5 ° C和10°C之间，这两种腺苷受体激活剂减少神经诱发的ACh释放的能力被阻止或大大减弱。这种低温抑制通过鸟嘌呤核苷酸结合蛋白（例如腺苷酸环化酶）与第二信使偶联的受体的活化。在这些实验条件下，单独的低温并没有显著改变诱发的ACh分泌。3细胞外Ca拮抗剂Mg对诱发的ACh释放的抑制，其直接作用于阻断Ca通道，不受低温的影响。4结果与温度敏感的第二信使系统控制与细胞外腺苷受体激活相关的细胞内事件的假设一致。
1A study was made to exclude the notion that adenosine receptor agonists exert a direct physical blockade of the depolarization‐secretion process. Reduced temperature was employed as a tool for distinguishing between physico‐chemical processes (such as those which mediate evoked transmitter release) and biochemical mechanisms (such as those which involve second messenger substances) in the action of adenosine. Adenosine and 2‐chloroadenosine were used as agonists in this electrophysiological study of the release of acetylcholine (ACh) from frog motor nerve terminals.2The ability of these two adenosine receptor activators to reduce neurally‐evoked ACh release was prevented or greatly attenuated by maintaining the preparation at temperatures between 5 and 10°C. Such low temperatures inhibit the activation of receptors coupled to second messengers via guanine nucleotide binding proteins (e.g. adenylate cyclase). Low temperature alone did not substantially alter evoked ACh secretion under the conditions of these experiments.3Inhibition of evoked ACh release by the extracellular Ca antagonist Mg, which acts directly to block Ca channels, was not affected by low temperature.4The results are consistent with the hypothesis that a temperature‐sensitive second messenger system controls the intracellular events linked to extracellular adenosine receptor activation.