Silverdale M A, Nicholson S L, Ravenscroft P, Crossman A R, Millan M J, Brotchie J M
Manchester Movement Disorder Laboratory, School of Biological Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK.
Exp Neurol. 2004 Jul;188(1):128-38. doi: 10.1016/j.expneurol.2004.03.022.
To date, the lack of highly selective antagonists at the dopamine D(3) receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D(3) versus D(2) receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D(3)-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses, S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D(3) receptor stimulation. Indeed, stimulation of D(3) receptors may be detrimental to the anti-parkinsonian properties of D(2)/D(3) agonists. Selectivity for stimulation of D(2), over D(3), receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.
迄今为止,由于缺乏多巴胺D(3)受体的高选择性拮抗剂,使得阐明其在帕金森病现有治疗方法作用机制中的作用受到阻碍。然而,新型苯并吡喃并吡咯化合物S33084作为D(3)受体拮抗剂,相对于D(2)受体及所有其他测试位点,表现出超过100倍的选择性。将S33084给予预先用左旋多巴引发异动症的1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)损伤的狨猴。单独给药时,S33084产生适度但显著的抗帕金森病作用,且不会引发异动症。在低D(3)选择性剂量(0.16和0.64mg/kg)下,S33084以不同程度和质的不同方式增强了罗匹尼罗和左旋多巴的抗帕金森病作用。在这些剂量下,S33084并未显著改变左旋多巴诱导的或罗匹尼罗诱导的异动症。这些数据表明,罗匹尼罗和左旋多巴并非通过刺激D(3)受体发挥其抗帕金森病或促异动症作用。事实上,刺激D(3)受体可能对D(2)/D(3)激动剂的抗帕金森病特性有害。因此,对D(2)受体而非D(3)受体刺激的选择性可能是多巴胺受体激动剂在治疗已出现异动症的帕金森病患者运动症状方面的有益特性。