Antkiewicz-Michaluk L, Michaluk J, Romańska I, Vetulani J
Department of Biochemistry, Polish Academy of Sciences, Krakow.
Eur J Pharmacol. 1990 May 3;180(1):129-35. doi: 10.1016/0014-2999(90)90600-b.
The density of cortical [3H]nitrendipine binding sites was elevated by over 40% in rats rendered morphine-abstinent by administration of naloxone after chronic treatment with morphine. The morphine-abstinent rats had significantly shortened response latencies in the hot-plate test. Nifedipine treatment abolished the signs of abstinence and normalized the hot-plate latencies in morphine-dependent, naloxone-treated rats. The results indicate that the symptoms of abstinence are related to a functional state of cortical dihydropyridine-sensitive calcium channels.
在用吗啡长期治疗后通过给予纳洛酮使大鼠产生吗啡戒断反应,此时皮质[3H]尼群地平结合位点的密度升高了40%以上。吗啡戒断大鼠在热板试验中的反应潜伏期显著缩短。硝苯地平治疗消除了吗啡依赖且经纳洛酮处理的大鼠的戒断症状,并使热板潜伏期恢复正常。结果表明,戒断症状与皮质二氢吡啶敏感性钙通道的功能状态有关。