D'Aquila Paolo S, Panin Francesca, Serra Gino
Dipartimento di Scienze del Farmaco, Università di Sassari, via Muroni 23/a, 07100 Sassari, Italy.
Eur J Pharmacol. 2006 Mar 27;535(1-3):208-11. doi: 10.1016/j.ejphar.2006.02.016. Epub 2006 Mar 14.
Based on experimental evidence suggesting a relationship between dopamine and mania, we proposed the antidepressant-induced dopaminergic supersensitivity as a model of antidepressant-related mania. We have previously shown the ability of carbamazepine, but not lithium, to prevent this phenomenon. Here we show that sodium valproate (50 mg/kg/day for 3 weeks) fails to prevent imipramine (20 mg/kg/day for 3 weeks)-induced sensitization to the locomotor response to the dopamine D2-like receptor agonist quinpirole (0.15 mg/kg). Since lithium, carbamazepine and valproate are all considered poorly effective in the treatment of antidepressant-related mania, the validity of the proposed model should be disproved by the carbamazepine results, to which, however, a pharmacokinetic mechanism might have concurred.
基于提示多巴胺与躁狂症之间存在关联的实验证据,我们提出抗抑郁药诱导的多巴胺能超敏反应作为抗抑郁药相关躁狂症的模型。我们之前已表明卡马西平而非锂能够预防这种现象。在此我们表明丙戊酸钠(50毫克/千克/天,持续3周)未能预防丙咪嗪(20毫克/千克/天,持续3周)诱导的对多巴胺D2样受体激动剂喹吡罗(0.15毫克/千克)的运动反应致敏。由于锂、卡马西平和丙戊酸钠在治疗抗抑郁药相关躁狂症方面均被认为效果不佳,所提出模型的有效性应由卡马西平的结果予以反驳,然而,药代动力学机制可能也对此有影响。