Application of raclopride PET in Parkinson's disease

闫卫红　

摘　要：帕金森病是发生于中年以上的中枢神经系统的变性疾病,由于多巴胺产生不足,引起多巴胺D2受体功能异常.Raclopride(雷氯必利)对中枢神经系统D2受体具有高度的选择性和亲和力,是研究D2受体分布的理想示踪剂.11C-raclopride PET可在分子水平直观地显示D2受体的分布、密度及变化情况,对帕金森病的病情分析、序列运动的多巴胺机制分析、运动波动合并症的机制分析、药物作用机制分析、外科治疗的机制分析等方面具有重要意义.
关键词：雷氯必利;帕金森病;受体,多巴胺D2;正电子发射型体层显像
分类号：R817.4　文献标识码：A
文章编号：1001-098X(2005)01-0027-03
 
作者单位：闫卫红（300052,天津医科大学总医院神经内科）　

参考文献：

[1]Hirvonen J, Aalto S, Lumme V, et al. Measurement of striatal and thalamic dopamine D2receptor binding with 11C-raclopride [J]. Nucl Med Commun, 2003, 24-(12): 1207-1214.
[2]Brooks DJ, Ibanez V, Sawle GV, et al. Striatal D2 receptor status in patients with Parkinson's disease, striatonigral degeneration, and progressive supranuclear palsy, measured with 11C-raclopride and positron emission tomography[J]. Ann Neurol, 1992, 31(2): 184-192.
[3]Rinne JO, Laihinen A, Rinne UK, et al. D2 receptor changes during the progression of early Parkinson's disease[J]. Mov Disord, 1993, 8 (2): 134-138.
[4]Rinne JO, Laihinen A, Ruottinen H, et al. Increased density of dopamine D2 receptors in the putamen, but not in the caudate nucleus in early Parkinson's disease: a PET study with [11C] raclopride[J]. J Neurol Sci, 1995, 132(2): 156-161.
[5]Turjanski N, Lees AJ, Brooks DJ. In vivo studies on striatal dopamine D1 and D2 site binding in L-dopa-treated Parkinson's disease patients with and without dyskinesias[J]. Neurology, 1997,49(3): 717-723.
[6]Sawle GV, Playford ED, Brooks DJ, et al. Asymmetricalpre-synap tic and post-synpatic changes in the striataldopamine projection in dopa naive parkinsonism: Diagnostic implications of the D2 receptor status[J]. Brain, 1993, 116 (4): 853-867.
[7]Antonini A, Schwarz J, Oertel WHr, et al. Long-term changes of striatal dopamine D2 receptors in patients with Parkinson's disease: a study with positron emission tomography and [11C]raclopride [J]. Mov Disord, 1997, 12(1): 33-38.
[8]Goerendt IK, Messa C, Lawrence AD, et al. Dopamine release duringsequential finger movements in health and Parkinson's disease: a PET study[J]. Brain, 2003, 126(2): 312-325.
[9]Ouchi Y, Yoshikawa E, Futatsubashi M, et al. Effect of simple motor performance on regional dopamine release in the striatum in Parkinson disease patients and healthy subjects: a positron emission tomog-raphy study[J]. J Cereb Blood Flow Metab, 2002, 22 (6): 746-752.
[10]Tedroff J, Pedersen M, Aquilonius SM, et al. Levodopa-induced changes in synaptic dopamine in patients with Parkinson's disease as measured by [11C] raclopride displacement and PET [J]. Neurology, 1996, 46(5): 1430-1436.
[11]Fuente-Fernandez R, Lu JQ, Sossi V, et al. Biochemical variations in the synaptic level of dopamine precede motor fluctuations in Parkinson's disease: PET evidence of increased dopamine turnover [J]. Ann Neurol, 2001, 49(3): 298-303.
[12]Linazasoro G, Obeso JA, Gomez JC, et al. Modification of dopamine D2 receptor activity by pergolide in Parkinson's disease: an in vivo study by PET[J]. Clin Neuropharmacol, 1999, 22(5):277-280.
[13]Moresco RM, Volonte MA, Messa C, et al. New perspectives on neurochemicaleffects of amantadine in the brain of parkinsonian patients: a PET-[(11)C]raclopride study[J]. J Neural Transm, 2002, 109(10): 1265-1274.
[14]Piccini P, Pavese N, Brooks DJ. Endogenous dopamine release after pharmacological challenges in Parkinson's disease[J]. Ann Neurol, 2003, 53(5): 647-653.
[15]Hilker R, Voges J, Ghaemi M, et al. Deep brain stimulation of the subthalamic nucleus does not increase the striatal dopamine concentration in parkinsonian humans[J]. Mov Disord, 2003, 18(1): 41-48.
[16]Piccini P, Brooks DJ, Bjorklund A, et al. Dopamine release from nigral transplants visualized in vivo in a Parkinson's patient[J]. Nat Neurosci, 1999, 2(12): 1137-1140.