Pennefather P, Puil E, Quastel D M
Can J Physiol Pharmacol. 1980 Oct;58(10):1221-8. doi: 10.1139/y80-185.
The coupling between nerve terminal depolarization and quantal secretion of acetylcholine at the mouse neuromuscular junction was estimated by measuring the multiplication of the frequency of miniature end-plate potentials (m.e.p.p.s) produced by increasing the concentration of calcium in the medium from 0.1 to 1.0 mM in the presence of 15 mM potassium. Depolarization-secretion coupling was inhibited by the anaesthetic steroids progesterone, pregnanedione, and alphaxalone. The nonanaesthetic steroid delta 16-alphaxalone also inhibited depolarization-secretion coupling with the same potency as alphaxalone. This results indicates that inhibition of depolarization-secretion coupling in nerve terminals is unlikely to play a major role in the production of anaesthesia.
通过在15 mM钾存在的情况下,将培养基中钙的浓度从0.1 mM增加到1.0 mM,测量微小终板电位(m.e.p.p.s)频率的倍增,来估计小鼠神经肌肉接头处神经末梢去极化与乙酰胆碱量子分泌之间的偶联。麻醉类固醇孕酮、孕烷二酮和alphaxalone可抑制去极化-分泌偶联。非麻醉类固醇δ16-alphaxalone也以与alphaxalone相同的效力抑制去极化-分泌偶联。这一结果表明,神经末梢去极化-分泌偶联的抑制在麻醉产生中不太可能起主要作用。