Damaj M I, Martin B R
Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0613.
Psychopharmacology (Berl). 1993;111(1):106-8. doi: 10.1007/BF02257415.
Pretreatment with ineffective doses of the D1 antagonist SCH23390 but not the D2 antagonist sulpiride reduced hyperactivity induced by nicotine in mice habituated to the test cage. On the other hand, the D1 and D2 antagonists were ineffective in blocking nicotine-induced hypoactivity in naive mice. Finally, SCH23390 and sulpiride did not block the antinociception induced by nicotine. Our data indicate that the dopamine receptors D1 and D2 are not involved in all the central effects of nicotine in mice, but seems to be a substrate for locomotor activation induced by nicotine under specific experimental conditions.
用无效剂量的D1拮抗剂SCH23390而非D2拮抗剂舒必利进行预处理,可降低习惯了测试笼环境的小鼠中尼古丁诱导的多动。另一方面,D1和D2拮抗剂对阻断尼古丁诱导的未适应小鼠的活动减少无效。最后,SCH23390和舒必利不能阻断尼古丁诱导的抗伤害感受。我们的数据表明,多巴胺受体D1和D2并不参与尼古丁在小鼠中的所有中枢效应,但似乎是特定实验条件下尼古丁诱导的运动激活的一个作用靶点。