On the mechanism by which adenosine receptor activation inhibits the release of acetylcholine from motor nerve endings.
On the mechanism by which adenosine receptor activation inhibits the release of acetylcholine from motor nerve endings.
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关于腺苷受体激活抑制运动神经末梢释放乙酰胆碱的机制。
DOI：
10.1113/jphysiol.1984.sp015019
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
E. M. Silinsky
中科院分区：
文献类型：
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作者：
E. M. Silinsky
研究了腺苷受体激动剂抑制蛙骨骼肌运动神经末梢乙酰胆碱（ACh）释放的过程。腺苷和2‐氯腺苷用作激动剂。每一种激动剂减少了响应神经冲动同步释放的ACh包的平均数量(m)。腺苷作为释放抑制剂的效力比2氯腺苷低一到两个数量级。局部记录的神经末梢动作电位不受任何腺苷受体激动剂的影响。在正常Ca （1.8 mM）中，添加足够的Mg使m降低到控制值的一半以下，并没有改变腺苷受体激动剂产生的抑制程度。不需要通过Ca通道（含Ca脂质体，La）进入的方法引起的乙酰胆碱释放被2氯腺苷或腺苷抑制。在含Ba的无Ca溶液中，两种腺苷受体激动剂均可抑制神经诱发的异步ACh释放（微型终板电位频率= m.e.p.p.f）的大小，但不改变m.e.p.p.f的衰减速率常数；m.e.p.p.f的衰减被认为反映了乙酰胆碱释放区Ba的清除速率。将钙从储存部位移出并抑制磷酸二酯酶的药物会在细胞外钙缺乏的情况下增加m.e.p.p.f，并增加腺苷受体激动剂产生的抑制水平。RMI 12,330A (7 X 10（‐6）至7 X 10（‐5）M)，腺苷酸环化酶抑制剂，阻断腺苷受体激动剂对乙酰胆碱释放的影响。结果与腺苷酸环化酶上的细胞外腺苷受体的激活通过降低细胞内分泌器官对Ca的亲和力来抑制乙酰胆碱释放的假设是一致的。
The process by which adenosine receptor agonists inhibit the evoked release of acetylcholine (ACh) was studied at motor nerve endings to frog skeletal muscle. Adenosine and 2‐chloroadenosine were employed as agonists. Each agonist reduced the mean number of ACh packets released synchronously in response to a nerve impulse (m). Adenosine was from one to two orders of magnitude less potent than 2‐chloroadenosine as an inhibitor of this release. Focally recorded nerve terminal action potentials were unaffected by either adenosine receptor agonist. In normal Ca (1.8 mM), addition of sufficient Mg to reduce m to less than half the control value did not alter the degree of inhibition produced by adenosine receptor agonists. ACh release evoked by methods that do not require Ca entry through Ca channels (Ca‐containing liposomes, La) was inhibited by either 2‐chloroadenosine or adenosine. In Ca‐free solutions containing Ba, the magnitude of neurally evoked asynchronous ACh release (miniature end‐plate potential frequency = m.e.p.p.f) was depressed by either adenosine receptor agonist without change in the rate constant of decay of m.e.p.p.f; the m.e.p.p.f decay is thought to reflect the rate of clearance of Ba from regions of ACh release. Agents which displace Ca from storage sites and also inhibit phosphodiesterases increased m.e.p.p.f in the virtual absence of extracellular Ca and increased the level of inhibition produced by adenosine receptor agonists. RMI 12,330A (7 X 10(‐6) to 7 X 10(‐5) M), an adenylate cyclase inhibitor, occluded the effects of adenosine receptor agonists on ACh release. The results are consistent with the hypothesis that activation of extracellular adenosine receptors on adenylate cyclase inhibits evoked ACh release by reducing the affinity for Ca of an intracellular component of the secretory apparatus.