Chenu F, Dailly E, Bourin M
Neurobiologie de l'Anxiété et de la Dépression, EA 3256, Faculté de Médecine, 1 rue Gaston Veil, 44035 Nantes Cedex, France.
Eur Neuropsychopharmacol. 2007 Feb;17(3):187-93. doi: 10.1016/j.euroneuro.2006.04.006. Epub 2006 Jun 6.
There is growing evidence suggesting that dopamine could be indirectly involved in the appearance of behavioural effects of antidepressants. In this study, we induced a partial (over 70%) and non-reversible depletion of dopamine-containing neurons in mice by i.c.v. infusion of 6-OHDA. Then, we compared the antidepressant-like effect of drugs (citalopram, paroxetine, desipramine and imipramine) with or without dopamine depletion in the mice forced swimming test. Our results clearly show that lesion with 6-OHDA does not modify the response of mice to desipramine and imipramine, whereas dopamine depletion abolished the antidepressant-like effect of citalopram and paroxetine. It could then be suggested that antidepressant-like effect of selective serotonin reuptake inhibitors (paroxetine and citalopram) in the mice FST requires the activation of dopaminergic pathways to occur.
越来越多的证据表明，多巴胺可能间接参与抗抑郁药行为效应的出现。在本研究中，我们通过脑室内注射6-羟基多巴胺（6-OHDA）诱导小鼠体内含多巴胺神经元部分（超过70%）且不可逆的耗竭。然后，我们在小鼠强迫游泳试验中比较了多巴胺耗竭与否的情况下药物（西酞普兰、帕罗西汀、地昔帕明和丙咪嗪）的抗抑郁样作用。我们的结果清楚地表明，6-OHDA损伤不会改变小鼠对地昔帕明和丙咪嗪的反应，而多巴胺耗竭则消除了西酞普兰和帕罗西汀的抗抑郁样作用。由此可以推测，选择性5-羟色胺再摄取抑制剂（帕罗西汀和西酞普兰）在小鼠强迫游泳试验中的抗抑郁样作用需要多巴胺能通路的激活才能发生。
