Shinozuka K, Maeda T, Hayashi E
Eur J Pharmacol. 1985 Jul 31;113(3):417-24. doi: 10.1016/0014-2999(85)90090-1.
The effects of adenosine on acetylcholine (ACh) release and calcium uptake were examined in a synaptosomal fraction prepared from guinea-pig ileum myenteric plexus-longitudinal muscle. A high concentration of potassium (40 mM) and electrical pulses (ES:10Hz) caused a marked increase in the output of [3H]ACh from [3H]choline-preloaded crude synaptosomes. This [3H]ACh output was calcium- and temperature-dependent. Adenosine reduced the high potassium-induced release significantly, and the electrically stimulated release completely. When the preparation was depolarized by high potassium or electrical pulses, the 45Ca uptake by synaptosomes was significantly enhanced. The uptake of 45Ca induced by high potassium was significantly reduced and that induced by electrical stimulation was completely abolished by adenosine. From these results, it may be suggested that adenosine inhibits neurotransmitter release by suppressing the presynaptic influx of calcium ion during depolarization of the cholinergic nerve terminals in guinea-pig ileum.
在从豚鼠回肠肌间神经丛 - 纵行肌制备的突触体组分中，研究了腺苷对乙酰胆碱（ACh）释放和钙摄取的影响。高浓度钾（40 mM）和电脉冲（ES：10Hz）导致[3H]胆碱预加载的粗制突触体中[3H]ACh的输出显著增加。这种[3H]ACh输出依赖于钙和温度。腺苷显著降低了高钾诱导的释放，并完全抑制了电刺激释放。当制备物被高钾或电脉冲去极化时，突触体对45Ca的摄取显著增强。腺苷显著降低了高钾诱导的45Ca摄取，并完全消除了电刺激诱导的摄取。从这些结果可以推测，腺苷通过抑制豚鼠回肠胆碱能神经末梢去极化期间突触前钙离子内流来抑制神经递质释放。
