AMPHETAMINE INDUCED 11C RACLOPRIDE DISPLACEMENT IN MOOD DISORDERS

安非他明引起心境障碍中的 11C 雷氯必利置换

• 批准号: 6264167
• 负责人: WAYNE C DREVETS
• 金额: $ 0.3万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-12-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6264167
• 关键词: amphetamines; clinical research; dopamine; drug interactions; human subject; major depression; mood disorders; neurochemistry; pharmacokinetics; positron emission tomography; raclopride

To access central dopaminergic function in major depressive disorder (MDD), PET measures of 11C raclopride uptake will be acquired at baseline, after amphetamine (AMPH) induced dopamine (DA) release and following a-methyl-para-tyrosine induced DA depletion in control and depressed samples. The 11C-raclopride uptake in these conditions will provide measure of the baseline dopamine D2/D3 receptor binding, the baseline occupancy of these receptors by endogenous DA and the amount of DA released following AMPH administration in each subject sample. These measures will be compared between depressives and controls to test the hypothesis that MDD is associated with a reduction in ventral striatal DA concentrations.

为了了解重度抑郁症（MDD）的中枢多巴胺能功能，将在基线、安非他明（AMPH）诱导多巴胺（DA）释放后和a-甲基-对酪氨酸诱导DA消耗后，在对照和抑郁样本中获得11C羟氯pride摄取的PET测量。在这些条件下11c -氯氯pride的摄取将提供多巴胺D2/D3受体结合的基线测量，内源性DA对这些受体的基线占用以及每个受试者样品中AMPH给药后DA的释放量。这些测量将在抑郁症患者和对照组之间进行比较，以验证MDD与腹侧纹状体DA浓度降低有关的假设。