Nomoto M, Jenner P, Marsden C D
MRC Movement Disorder Research Group, University Department of Neurology, London, U.K.
Neurosci Lett. 1988 Nov 11;93(2-3):275-80. doi: 10.1016/0304-3940(88)90095-x.
Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits. Administration of the D1 agonist SKF 38393 (2.5-20 mg/kg, i.p.) caused a dose-dependent increase of this akinesia. Administration of the D2 agonist LY 171555 (0.3 mg/kg, i.p.) reversed the motor deficits induced by MPTP treatment. Pretreatment of animals with SKF 38393 (2.5-20 mg/kg, i.p.) caused dose-dependent inhibition of the anti-parkinsonian action of LY 171555 (0.3 mg/kg i.p.). In primates SKF 38393 does not reverse motor deficits induced by MPTP and inhibits the actions of a D2-agonist.
给普通狨猴注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)会导致持续性运动功能障碍。注射D1激动剂SKF 38393(2.5 - 20毫克/千克,腹腔注射)会使这种运动不能呈剂量依赖性增加。注射D2激动剂LY 171555(0.3毫克/千克,腹腔注射)可逆转MPTP治疗引起的运动功能障碍。用SKF 38393(2.5 - 20毫克/千克,腹腔注射)对动物进行预处理会导致LY 171555(0.3毫克/千克,腹腔注射)的抗帕金森作用呈剂量依赖性抑制。在灵长类动物中,SKF 38393不能逆转MPTP诱导的运动功能障碍,并且会抑制D2激动剂的作用。