Jeziorski M, White F J
Department of Neuroscience, Finch University of Health Sciences, Chicago Medical School, IL 60064-3095, USA.
Eur J Pharmacol. 1995 Mar 14;275(3):235-44. doi: 10.1016/0014-2999(94)00779-7.
The present experiments determined the effects of selective dopamine receptor antagonists on the initiation and expression of sensitization to the locomotor-stimulating effects of morphine in rats. Although both the dopamine D1 receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzaz epine hydrochloride (SCH 23390, 0.25 mg/kg) and the dopamine D2 receptor antagonist eticlopride (0.1 mg/kg) suppressed the ability of morphine (10 mg/kg) to elicit sensitized locomotor activity during the course of a 12 day treatment schedule, subsequent tests with morphine alone revealed significant sensitization. Sensitization in the SCH 23390 + morphine group could not be attributed to dopamine D1 receptor supersensitivity caused by repeated SCH 23390 administration because electrophysiological recordings indicated that nucleus accumbens neurons in SCH 23390-treated rats were not more sensitive to the inhibitory effects of either dopamine or a dopamine D1 receptor-selective agonist. Thus, dopamine receptor stimulation may be involved in expression, but not development, of morphine sensitization.
本实验确定了选择性多巴胺受体拮抗剂对大鼠吗啡运动刺激作用敏化的起始和表达的影响。虽然多巴胺D1受体拮抗剂R(+)-7-氯-8-羟基-3-甲基-1-苯基-2,3,4,5-四氢-1H-3-苯并氮杂卓盐酸盐（SCH 23390，0.25毫克/千克）和多巴胺D2受体拮抗剂依托必利（0.1毫克/千克）在12天的治疗过程中均抑制了吗啡（10毫克/千克）引发敏化运动活性的能力，但随后单独使用吗啡的测试显示出明显的敏化现象。SCH 23390 + 吗啡组的敏化不能归因于重复给予SCH 23390导致的多巴胺D1受体超敏反应，因为电生理记录表明，接受SCH 23390治疗的大鼠伏隔核神经元对多巴胺或多巴胺D1受体选择性激动剂的抑制作用并不更敏感。因此，多巴胺受体刺激可能参与吗啡敏化的表达，但不参与其形成。
