皮质切片中的吗啡戒断：Ca2+通道抑制剂对戒断诱导的[3H]-去甲肾上腺素释放的抑制作用
Morphine withdrawal in cortical slices: suppression by Ca2+-channel inhibitors of abstinence-induced [3H]-noradrenaline release.
作者信息
Pellegrini-Giampietro D E, Bacciottini L, Carlà V, Moroni F
机构信息
Department of Preclinical and Clinical Pharmacology Mario Aiazzi Mancini, University of Florence, Firenze, Italy.
出版信息
Br J Pharmacol. 1988 Mar;93(3):535-40. doi: 10.1111/j.1476-5381.1988.tb10308.x.
Abstract
- The effects of morphine withdrawal were evaluated in vitro by monitoring the actions of naloxone on the depolarization-induced release of [3H]-noradrenaline (NA) in cortical slices taken from naïve or dependent rats. The effects of dihydropyridine molecules acting on Ca2+-channels (nimodipine and Bay K 8644) were also studied in this model. 2. Naloxone (10(-8)-10(-5) M) dose-dependently enhanced the K+ induced release of [3H]-NA in slices taken from dependent rats, but failed to modify the [3H]-NA release from 'naïve' slices. 3. The naloxone-induced potentiation of release was significantly reversed by nimodipine (10(-8)-10(-6) M). These doses of nimodipine did not change [3H]-NA release (both basal and K+ induced) in preparations obtained from naïve rats. 4. Bay K 8644 potentiated the K+-induced [3H]-NA release from cortical slices taken from naïve rats to a similar extent as that of naloxone in dependent rats. 5. These results suggest that the naloxone potentiation of the depolarization-induced [3H]-NA release in slices taken from dependent rats may be considered a model of morphine withdrawal in vitro. In this model dihydropyridine Ca2+-channel antagonists suppress morphine-withdrawal effects in a similar manner to observations made in vivo.
摘要
- 通过监测纳洛酮对取自未接触过吗啡或已产生依赖性大鼠的皮质切片中去极化诱导的[3H]-去甲肾上腺素（NA）释放的作用，在体外评估吗啡戒断的影响。还在此模型中研究了作用于Ca2+通道的二氢吡啶分子（尼莫地平和Bay K 8644）的影响。2. 纳洛酮（10(-8)-10(-5) M）剂量依赖性地增强了取自依赖性大鼠切片中K+诱导的[3H]-NA释放，但未能改变“未接触过吗啡”切片中[3H]-NA的释放。3. 尼莫地平（10(-8)-10(-6) M）可显著逆转纳洛酮诱导的释放增强作用。这些剂量的尼莫地平在取自未接触过吗啡大鼠的制剂中不会改变[3H]-NA释放（基础释放和K+诱导释放）。4. Bay K 8644增强了取自未接触过吗啡大鼠皮质切片中K+诱导的[3H]-NA释放，其程度与纳洛酮对依赖性大鼠的作用相似。5. 这些结果表明，纳洛酮增强取自依赖性大鼠切片中去极化诱导的[3H]-NA释放可被视为体外吗啡戒断的模型。在此模型中，二氢吡啶Ca2+通道拮抗剂以与体内观察结果相似的方式抑制吗啡戒断效应。
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