Henderson G, North R A
Br J Pharmacol. 1976 Jul;57(3):341-6.
1 Intracellular recordings were made from smooth muscle cells of the mouse vas deferens. Excitatory junction potentials (e.j.ps) were evoked by stimulation of the intramural nerves. 2 Normorphine (50 nM-5muM) depressed the amplitude of the e.j.p. The ED50 was 430 nM. The latency of the e.j.p. and the resting membrane potential of the smooth muscle cells were unaffected by normorphine. 3 The depression of the e.j.p. by narcotic analgesic drugs was stereospecific. 4 Naloxone (100 nM) completely reversed the depression of the e.j.p. produced by normorphine (1 muM). Naloxone (100 nM) alone did not alter the amplitude of the e.j.p. 5 Normorphine (1 muM) did not prevent the depolarization of the smooth muscle cells produced by exogenous noradrenaline (10 muM). 6 It is concluded that narcotic analgesic drugs act directly upon the transmitter release sites to reduce the amount of noradrenaline liberated by each nerve impulse.
从小鼠输精管的平滑肌细胞进行细胞内记录。通过刺激壁内神经诱发兴奋性接头电位(e.j.p.s)。
去甲吗啡(50 nM - 5μM)降低了e.j.p.的幅度。半数有效剂量(ED50)为430 nM。e.j.p.的潜伏期和平滑肌细胞的静息膜电位不受去甲吗啡影响。
麻醉性镇痛药对e.j.p.的抑制具有立体特异性。
纳洛酮(100 nM)完全逆转了去甲吗啡(1μM)对e.j.p.的抑制作用。单独使用纳洛酮(100 nM)不会改变e.j.p.的幅度。
去甲吗啡(1μM)不能阻止外源性去甲肾上腺素(10μM)引起的平滑肌细胞去极化。
得出结论,麻醉性镇痛药直接作用于递质释放部位,以减少每次神经冲动释放的去甲肾上腺素量。