Kuribara H
Department of Neurobiology and Behavior, Gunma University School of Medicine, Maebashi, Japan.
Pharmacol Biochem Behav. 1995 Dec;52(4):759-63. doi: 10.1016/0091-3057(95)00173-t.
SCH 23390 [0.003-0.03 mg/kg, subcutaneously (SC)], a dopamine D1 receptor antagonist, dose-dependently inhibited the ambulation-stimulant effect of methamphetamine (MAP) (2 mg/kg, SC) in mice when two drugs were combined in repeated administrations at 3- to 4-day intervals, repeated five times. SCH 23390 (0.03 mg/kg), which was sufficient to abolish the acute effect of MAP completely throughout the repeated administrations, significantly inhibited the induction of MAP sensitization. Moreover, when the mice were posttreated with SCH 23390 (0.01 and 0.03 mg/kg) 3 h after each MAP administration, at which the ambulation-stimulant effect of MAP had almost disappeared, they showed a significant and dose-dependent retardation of the induction of MAP sensitization. However, the 24-h posttreatment with SCH 23390 had no such effect. The administration of SCH 23390 (0.003-0.03 mg/kg) alone in either the activity cage or the home cage, or saline in the activity cage with 3- or 24-h posttreatment with SCH 23390 (0.01 or 0.03 mg/kg) five times at 3- to 4-day intervals did not elicit any significant changes in MAP sensitivity. The present results indicate that an intense blockade of dopamine D1 receptors in the acute or subacute period after MAP administration causes retardation of MAP sensitization by means of ambulation in mice.
SCH 23390（0.003 - 0.03毫克/千克，皮下注射），一种多巴胺D1受体拮抗剂，当两种药物以3至4天的间隔重复给药五次时，能剂量依赖性地抑制甲基苯丙胺（MAP，2毫克/千克，皮下注射）对小鼠的行走刺激作用。在整个重复给药过程中足以完全消除MAP急性作用的SCH 23390（0.03毫克/千克），显著抑制了MAP敏感性的诱导。此外，在每次MAP给药后3小时用SCH 23390（0.01和0.03毫克/千克）对小鼠进行后处理时，此时MAP的行走刺激作用几乎消失，它们表现出MAP敏感性诱导的显著且剂量依赖性的延迟。然而，用SCH 23390进行24小时后处理没有这种效果。在活动笼或饲养笼中单独给予SCH 23390（0.003 - 0.03毫克/千克），或者在活动笼中给予生理盐水并以3至4天的间隔用SCH 23390（0.01或0.03毫克/千克）进行五次3小时或24小时后处理，均未引起MAP敏感性的任何显著变化。目前的结果表明，在MAP给药后的急性或亚急性期强烈阻断多巴胺D1受体会通过小鼠的行走导致MAP敏感性的延迟。
