Marien M, Briley M, Colpaert F
Division Neurobiologie I, Centre de Recherche Pierre Fabre, Castres, France.
Eur J Pharmacol. 1993 Jun 4;236(3):487-9. doi: 10.1016/0014-2999(93)90489-5.
Injection of C57Bl/6 mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 4 x 10 mg/kg i.p. over 8 h) resulted in a partial (40%) striatal dopamine depletion at 7 days post-drug. Pretreatment with the selective noradrenergic neurotoxin N-[2-chloroethyl]-N-ethyl-2-bromobenzylamine (DSP-4; 40 mg/kg i.p.), while having no effect per se on striatal dopamine levels, exacerbated the MPTP-induced dopamine deficit to 60%. Results support the hypothesis that damage to the locus coeruleus-noradrenergic system, by removing a facilitatory influence on the nigrostriatal dopamine system, interferes with the ability of the nigrostriatal pathway to compensate for or recover from injury.
给C57Bl/6小鼠腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP；8小时内腹腔注射4×10毫克/千克），在给药后7天导致纹状体多巴胺部分（40%）耗竭。用选择性去甲肾上腺素能神经毒素N-[2-氯乙基]-N-乙基-2-溴苄胺（DSP-4；40毫克/千克腹腔注射）预处理，虽然其本身对纹状体多巴胺水平没有影响，但使MPTP诱导的多巴胺缺乏加剧至60%。结果支持这样的假说，即通过消除对黑质纹状体多巴胺系统的促进作用，蓝斑-去甲肾上腺素能系统的损伤会干扰黑质纹状体通路从损伤中补偿或恢复的能力。
