Nordquist R E, Risterucci C, Moreau J L, von Kienlin M, Künnecke B, Maco M, Freichel C, Riemer C, Spooren W
CNS Research, F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland.
Neuropharmacology. 2008 Feb;54(2):405-16. doi: 10.1016/j.neuropharm.2007.10.010. Epub 2007 Oct 26.
Aripiprazole (OPC-14597) is an antipsychotic with a unique pharmacology as a dopamine D2 receptor partial agonist, which has been demonstrated to reduce symptoms of schizophrenia. To further profile this compound in preclinical models, we examined aripiprazole-induced activity changes as measured by pharmacological magnetic resonance imaging (MRI) and characterized the drug in several rodent models of motor behaviors and of psychosis. Continuous arterial spin labeling MRI measuring blood perfusion (as an indirect measure of activity) reveals that aripiprazole dose-dependently decreased brain activity in the entorhinal piriform cortex, perirhinal cortex, nucleus accumbens shell, and basolateral amygdala. While no deficits were observed in the rotarod test for motor coordination in the simpler (8 RPM) version, in the more challenging condition (16 RPM) doses of 10 and 30mg/kg i.p. produced deficits. Catalepsy was seen only at the highest dose tested (30mg/kg i.p.) and only at the 3 and 6h time points, not at the 1h time point. In pharmacological models of psychosis, 1-30mg/kg aripiprazole i.p. effectively reduced locomotor activity induced by dopamine agonists (amphetamine and apomorphine), NMDA antagonists (MK-801 and phencyclidine (PCP)), and a serotonin agonist (2,5-dimethoxy-4-iodoamphetamine (DOI)). However, aripiprazole reversed prepulse inhibition deficits induced by amphetamine, but not by any of the other agents tested. Aripiprazole alters brain activity in regions relevant to schizophrenia, and furthermore, has a pharmacological profile that differs for the two psychosis models tested and does not match the typical or atypical psychotics. Thus, D2 partial agonists may constitute a new group of antipsychotics.
阿立哌唑(OPC - 14597)是一种具有独特药理学特性的抗精神病药物,作为多巴胺D2受体部分激动剂,已被证明可减轻精神分裂症症状。为了在临床前模型中进一步研究该化合物,我们通过药理磁共振成像(MRI)检测了阿立哌唑诱导的活动变化,并在几种运动行为和精神病的啮齿动物模型中对该药物进行了表征。连续动脉自旋标记MRI测量脑血流灌注(作为活动的间接指标)显示,阿立哌唑剂量依赖性地降低了内嗅梨状皮质、嗅周皮质、伏隔核壳和基底外侧杏仁核的脑活动。在较简单的(8转/分钟)版本的转棒试验中未观察到运动协调缺陷,但在更具挑战性的条件(16转/分钟)下,腹腔注射10和30mg/kg剂量会产生缺陷。僵住症仅在测试的最高剂量(腹腔注射30mg/kg)下以及仅在3小时和6小时时间点出现,1小时时间点未出现。在精神病药理学模型中,腹腔注射1 - 30mg/kg阿立哌唑可有效降低多巴胺激动剂(苯丙胺和阿扑吗啡)、NMDA拮抗剂(MK - 801和苯环利定(PCP))以及5 - 羟色胺激动剂(2,5 - 二甲氧基 - 4 - 碘苯丙胺(DOI))诱导的运动活动。然而,阿立哌唑可逆转苯丙胺诱导的前脉冲抑制缺陷,但不能逆转其他任何测试药物诱导的缺陷。阿立哌唑改变了与精神分裂症相关区域的脑活动,此外,在所测试的两种精神病模型中具有不同药理学特征,且与典型或非典型抗精神病药物不匹配。因此,D2部分激动剂可能构成一类新的抗精神病药物。