Cherubini E, Morita K, North R A
Br J Pharmacol. 1984 Apr;81(4):617-22. doi: 10.1111/j.1476-5381.1984.tb16126.x.
Intracellular recordings were made from myenteric neurones removed from guinea-pig ileum and maintained in vitro. Action potentials were elicited by passing brief depolarizing currents through the recording electrode. In AH cells they were followed by afterhyperpolarizations resulting from an increase in potassium conductance (GK,Ca). Morphine (1 nM - 1 microM), applied by superfusion, increased the duration of the afterhyperpolarization (and the underlying GK,Ca) which followed from 1 to 30 action potentials. Morphine did not change the peak amplitude of the afterhyperpolarization. This action of morphine occurred both in cells which showed no change in resting membrane potential or resistance and in cells which were hyperpolarized. It was prevented by naloxone (10 nM - 1 microM). The possibility is proposed that morphine inhibits one of the mechanisms by which myenteric neurones control their free intracellular calcium concentration close to the plasma membrane.
从豚鼠回肠分离并在体外培养的肠肌间神经元进行了细胞内记录。通过记录电极施加短暂的去极化电流来诱发动作电位。在AH细胞中，动作电位之后是由于钾电导（GK,Ca）增加而导致的超极化后电位。通过灌流施加的吗啡（1 nM - 1 microM）增加了超极化后电位（以及潜在的GK,Ca）的持续时间，该持续时间从1到30个动作电位不等。吗啡没有改变超极化后电位的峰值幅度。吗啡的这种作用在静息膜电位或电阻没有变化的细胞以及超极化的细胞中均会出现。它被纳洛酮（10 nM - 1 microM）所阻断。有人提出，吗啡抑制了肠肌间神经元控制其靠近质膜的细胞内游离钙浓度的一种机制。
