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AMPHETAMINE INDUCED 11C RACLOPRIDE DISPLACEMENT IN MOOD DISORDERS

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:
6304640
负责人:
WAYNE C DREVETS
金额:
$0.3万
依托单位国家:
美国
项目类别:
财政年份:
1999
资助国家:
美国
项目状态:
已结题
起止时间:
1999-12-01 至 2000-11-30

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中文摘要
翻译
本研究的目的是评估重度抑郁症(MDD)的中枢多巴胺能功能。在对照和抑郁样本中,在安非他明(AMPH)诱导多巴胺(DA)释放和a-甲基-对酪氨酸(aMPT)诱导DA消耗后,将在基线时获得[11C]-raclopride摄取的PET测量。在这些条件下11c -氯氯pride的摄取将提供基线多巴胺D2/D3受体结合的测量,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。
英文摘要
The objective of this study is to assess 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 (aMPT) induced DA depletion in control and depressed samples. The 11C-raclopride uptake in these conditions will provide measures 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.
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