Department of Radiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
Synapse. 2011 Oct;65(10):991-7. doi: 10.1002/syn.20926. Epub 2011 Apr 26.
In a recent positron emission tomography (PET) study, we demonstrated the ability to measure amphetamine-induced dopamine (DA) release in the human cortex with the DA D₂/₃ radioligand [¹¹C]FLB 457. As previous studies in animals have shown that a relatively high fraction of the [¹¹C]FLB 457 signal in the cerebellum represents specific binding to D₂/₃ receptors, there was concern that the use of the cerebellum as a measure of nonspecific binding (i.e., reference region) to derive [¹¹C]FLB 457 binding potential (BP) (BP(ND) ) would bias cortical DA release measurements. Thus, we evaluated the fractional contribution of specific binding to D₂/₃ receptors in the human cerebellum for [¹¹C]FLB 457. Six healthy human subjects (5M/1F) were studied twice with [¹¹C]FLB 457, once at baseline and again following a single oral dose of 15 mg of aripiprazole, a D₂/₃ partial agonist. [¹¹C]FLB 457 distribution volume (V(T) ) was estimated using kinetic analysis in the cortical regions of interest and potential reference regions. The change in [¹¹C]FLB 457 V(T) following aripiprazole ranged from -33 to -42% in the cortical regions of interest (ROIs). The aripiprazole-induced change in [¹¹C]FLB 457 V(T) in three potential reference regions suggests significant specific binding the cerebellum (CER, -17 ± 12%), but not pons (PON, -10 ± 10%) and centrum semiovale (CESVL, -3 ± 12%). Nevertheless, a reanalysis of the published [¹¹C]FLB 457 test-retest and amphetamine studies suggests that the use of the PON V(T) and CESVL V(T) as an estimate of nonspecific binding to derive [¹¹C]FLB 457 BP(ND) in DA release studies is unlikely to be successful because it leads to less reproducible outcome measures, which in turn diminishes the ability to measure DA release in the cortex. D₂/₃ blocking studies with aripiprazole and [¹¹C]FLB 457 suggest specific binding to D₂/₃ receptors in the cerebellum. These data also suggest that the contribution of specific binding to D₂/₃ receptors in the cerebellum is lower than that in the cortical ROIs and that CER V(T) is mostly representative of nonspecific binding. Nevertheless, caution is advised when using reference tissue methods that rely solely on the cerebellum signal as an input function to quantify [¹¹C]FLB 457 BP(ND).
在最近的一项正电子发射断层扫描(PET)研究中,我们证明了使用多巴胺 D₂/₃放射性配体 [¹¹C]FLB 457 测量人类皮质中安非他命诱导的多巴胺(DA)释放的能力。由于先前的动物研究表明,小脑中的 [¹¹C]FLB 457 信号的相当大一部分代表对 D₂/₃受体的特异性结合,因此有人担心使用小脑作为非特异性结合(即参考区)来推导 [¹¹C]FLB 457 结合潜力(BP)(BP(ND))会使皮质 DA 释放测量产生偏差。因此,我们评估了 [¹¹C]FLB 457 在人类小脑中的特异性结合到 D₂/₃受体的分数贡献。6 名健康的人类受试者(5M/1F)接受了两次 [¹¹C]FLB 457 研究,一次是在基线时,另一次是在单次口服 15 毫克阿立哌唑后,阿立哌唑是一种 D₂/₃部分激动剂。使用皮质感兴趣区和潜在参考区的动力学分析来估计 [¹¹C]FLB 457 的分布容积(V(T))。在皮质感兴趣区(ROI)中,阿立哌唑引起的 [¹¹C]FLB 457 V(T)变化范围为-33%至-42%。在三个潜在参考区中,阿立哌唑诱导的 [¹¹C]FLB 457 V(T)变化表明小脑有明显的特异性结合(CER,-17±12%),但桥脑(PON,-10±10%)和半卵圆中心(CESVL,-3±12%)没有。尽管如此,对已发表的 [¹¹C]FLB 457 测试-重测和安非他命研究的重新分析表明,使用 PON V(T)和 CESVL V(T)作为估计非特异性结合来推导 DA 释放研究中的 [¹¹C]FLB 457 BP(ND)不太可能成功,因为它导致更不可复制的结果衡量标准,这反过来又降低了测量皮质中 DA 释放的能力。阿立哌唑和 [¹¹C]FLB 457 的 D₂/₃ 阻断研究表明小脑中有特异性结合到 D₂/₃ 受体。这些数据还表明,小脑中 D₂/₃ 受体的特异性结合的贡献低于皮质 ROI 中的贡献,并且 CER V(T)主要代表非特异性结合。尽管如此,当使用仅依赖小脑信号作为输入函数来量化 [¹¹C]FLB 457 BP(ND)的参考组织方法时,仍需谨慎。