Martin M I, Lizasoain I, Leza J C
Instituto de Farmacologia y Toxicologia, Facultad de Medicina, Universidad Complutense de Madrid, Spain.
Psychopharmacology (Berl). 1990;101(2):267-70. doi: 10.1007/BF02244138.
Acute morphine treatment has been shown to cause a uniform calcium depletion in various brain regions and to evoke hypermotility in mice. On the other hand, it has been reported previously that calcium channel blockers reduce the behavioral stimulation induced by different methods in mice, and it is known that these drugs increase the morphine analgesia and reduce the abstinence syndrome. The effect of calcium channel blockers, nifedipine and diltiazem, on the morphine- and amphetamine-induced hypermotility were evaluated. Mice activity was measured with photocell motility meters. The results show that neither nifedipine nor diltiazem decrease significantly the motility in control and amphetamine-treated mice; however, when they were administered to morphine-treated mice the hypermotility was significantly reduced. The mechanism responsible for this interference is still unknown.
急性吗啡治疗已被证明会导致不同脑区出现均匀的钙耗竭,并诱发小鼠运动亢进。另一方面,此前有报道称钙通道阻滞剂可减少小鼠中不同方法诱导的行为刺激,并且已知这些药物可增强吗啡镇痛作用并减轻戒断综合征。评估了钙通道阻滞剂硝苯地平和地尔硫䓬对吗啡和苯丙胺诱导的运动亢进的影响。用光电细胞运动计测量小鼠活动。结果表明,硝苯地平和地尔硫䓬均未显著降低对照小鼠和苯丙胺处理小鼠的运动性;然而,当将它们给予吗啡处理的小鼠时,运动亢进显著降低。这种干扰的机制仍然未知。