Diana M, Collu M, Mura A, Gessa G L
B.B. Brodie Department of Neuroscience, University of Cagliari, Italy.
Eur J Pharmacol. 1992 Feb 18;211(3):415-9. doi: 10.1016/0014-2999(92)90400-x.
Chronic treatment of rats with haloperidol (1 mg/kg twice daily for 4 weeks) induced repetitive vacuous chewing movements (VC), that persisted for over 72 h after haloperidol withdrawal. Haloperidol-induced VC were inhibited by the s.c. administration of the specific dopamine D1, receptor antagonist, SCH 23390 (0.025-0.100 mg/kg), in a dose-dependent manner, and were totally suppressed by an acute challenge with haloperidol (2 mg/kg i.p.) and by the dopamine synthesis inhibitor, alpha-methyl-tyrosine (AMT) (200 mg/kg i.p.). In AMT-treated rats, VC were reinstated by the administration of the selective D1 agonist, SKF 38393. The results support the hypothesis that chronic haloperidol-induced VC are mediated by dopamine acting selectively upon D1 receptors.
用氟哌啶醇对大鼠进行长期治疗（每天两次，每次1毫克/千克，持续4周）会诱发重复性的空嚼运动（VC），这种运动在停用氟哌啶醇后持续超过72小时。皮下注射特异性多巴胺D1受体拮抗剂SCH 23390（0.025 - 0.100毫克/千克）可剂量依赖性地抑制氟哌啶醇诱发的VC，而氟哌啶醇（2毫克/千克腹腔注射）和多巴胺合成抑制剂α-甲基酪氨酸（AMT）（200毫克/千克腹腔注射）的急性激发可完全抑制该运动。在接受AMT治疗的大鼠中，给予选择性D1激动剂SKF 38393可恢复VC。这些结果支持以下假说：长期氟哌啶醇诱发的VC是由多巴胺选择性作用于D1受体介导的。
