Batista Luara A, Viana Thércia G, Silveira Vívian T, Aguiar Daniele C, Moreira Fabrício A
Graduate School in Neuroscience, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Av. Pres. Antônio Carlos 6627, Belo Horizonte, MG, 31270-901, Brazil.
Naunyn Schmiedebergs Arch Pharmacol. 2016 Jan;389(1):11-6. doi: 10.1007/s00210-015-1170-x. Epub 2015 Aug 29.
Aripiprazole is an antipsychotic that acts as a partial agonist at dopamine D2 receptors. In addition to its antipsychotic activity, this compound blocks the effects of some psychostimulant drugs. It has not been verified, however, if aripiprazole interferes with the effects of caffeine. Hence, this study tested the hypothesis that aripiprazole prevents caffeine-induced hyperlocomotion and investigated the effects of these drugs on neural activity in the striatum. Male Swiss mice received injections of vehicle or antipsychotic drugs followed by vehicle or caffeine. Locomotion was analyzed in a circular arena and c-Fos protein expression was quantified in the dorsolateral, dorsomedial, and ventrolateral striatum, and in the core and shell regions of nucleus accumbens. Aripiprazole (0.1, 1, and 10 mg/kg) prevented caffeine (10 mg/kg)-induced hyperlocomotion at doses that do not change basal locomotion. Haloperidol (0.01, 0.03, and 0.1 mg/kg) also decreased caffeine-induced hyperlocomotion at all doses, although at the two higher doses, this compound reduced basal locomotion. Immunohistochemistry analysis showed that aripiprazole increases c-Fos protein expression in all regions studied, whereas caffeine did not alter c-Fos protein expression. Combined treatment of aripiprazole and caffeine resulted in a decrease in the number of c-Fos positive cells as compared to the group receiving aripiprazole alone. In conclusion, aripiprazole prevents caffeine-induced hyperlocomotion and increases neural activation in the striatum. This latter effect is reduced by subsequent administration of caffeine. These results advance our understanding on the pharmacological profile of aripiprazole.
阿立哌唑是一种抗精神病药物,它在多巴胺D2受体上作为部分激动剂发挥作用。除了其抗精神病活性外,该化合物还能阻断一些精神兴奋药物的作用。然而,阿立哌唑是否会干扰咖啡因的作用尚未得到证实。因此,本研究检验了阿立哌唑可预防咖啡因诱导的运动亢进这一假设,并研究了这些药物对纹状体神经活动的影响。雄性瑞士小鼠接受注射溶剂或抗精神病药物,随后注射溶剂或咖啡因。在圆形场地中分析运动情况,并对背外侧、背内侧和腹外侧纹状体以及伏隔核的核心和壳区域中的c-Fos蛋白表达进行定量。阿立哌唑(0.1、1和10mg/kg)在不改变基础运动的剂量下可预防咖啡因(10mg/kg)诱导的运动亢进。氟哌啶醇(0.01、0.03和0.1mg/kg)在所有剂量下也可降低咖啡因诱导的运动亢进,不过在两个较高剂量下,该化合物会降低基础运动。免疫组织化学分析表明,阿立哌唑可增加所有研究区域中的c-Fos蛋白表达,而咖啡因并未改变c-Fos蛋白表达。与单独接受阿立哌唑的组相比,阿立哌唑和咖啡因联合治疗导致c-Fos阳性细胞数量减少。总之,阿立哌唑可预防咖啡因诱导的运动亢进并增加纹状体中的神经激活。随后给予咖啡因可降低后一种效应。这些结果推进了我们对阿立哌唑药理特性的理解。