In vivo imaging of corticotropin releasing factor-nociceptin receptor interactions

基础研究假设，调节压力和压力的神经递质和 抗应激系统是负面强化和成瘾复发的基础。伤害素，它结合 对于伤害素/孤儿FQ肽(NOP)受体，就是这样一种神经肽递质 通过对抗促肾上腺皮质激素释放因子的功能作用发挥其抗应激作用 (CRF)，大脑中主要的应激调节神经肽递质。基础调查 提示CRF和伤害素分别促进和抑制类焦虑行为。收敛 这是来自酒精中毒动物模型的数据，这些动物模型支持CRF增加和减少 杏仁核延长区的伤害素水平是焦虑样行为的原因 沉溺于毒瘾。CRF1受体拮抗剂的能力进一步支持了这一假设 和NOP受体激动剂，以减弱酒精对一系列 上瘾的行为。因此，开发一种检查慢性肾功能衰竭的方法是相当有意义的。 人类吸毒者中的NOP相互作用。在这里，我们将用[11C]NOP-1A和[11C]NOP-1A在健康人身上进行评估 氢化可的松诱导的杏仁核CRF增加是否导致NOP受体改变 有约束力的。这项实验将首次记录CRF和NOP之间的体内相互作用， 并为今后评估这种互动在成瘾中是否异常奠定了基础 调查。 好了！

Basic investigations postulate that an imbalance between neurotransmitters regulating the stress and anti-stress systems underlie negative reinforcement and relapse in addiction. Nociceptin, which binds to the nociceptin/orphanin FQ peptide (NOP) receptor, is one such neuropeptide transmitter that exerts its anti-stress effects by counteracting the functional effects of corticotropin releasing factor (CRF), the primary stress-mediating neuropeptide transmitter in the brain. Basic investigations suggest that CRF and nociceptin facilitate and inhibit anxiety-like behaviors respectively. Convergent with this is data from animal models of alcoholism that support increased CRF and decreased nociceptin levels in the extended amygdala as the reason for anxiety-like behaviors that underlie relapse in addiction. This postulation is further supported by the ability of CRF1 receptor antagonists and NOP receptor agonists to blunt the reinforcing and motivational effects of alcohol on a range of addictive behaviors. Thus, it is of considerable interest to develop a methodology to examine CRF- NOP interactions in human addicts. Here, we will evaluate in healthy humans with [11C]NOP-1A and PET whether hydrocortisone-induced increases in amygdala CRF leads to altered NOP receptor binding. This experiment will for the first time document an in vivo interaction between CRF and NOP, and set the stage for evaluating whether this interaction is abnormal in addiction in future investigations. !