Department of Pharmacology, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Anesthesiology and Clinical Physiology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8549, Japan.
Psychopharmacology (Berl). 2019 Dec;236(12):3655-3665. doi: 10.1007/s00213-019-05337-6. Epub 2019 Jul 24.
Bupropion is used for major depressive disorder, smoking cessation aid, and obesity. It blocks reuptake of dopamine and noradrenaline and antagonizes nicotinic acetylcholine receptor. Animal studies showed that bupropion enhanced rewarding effects. In addition, bupropion has the potential to treat patients with reward processing dysfunction. However, neural substrates underlying the bupropion effects on reward function in human subjects are not fully understood.
We investigated single-dose administration of bupropion on neural response of reward anticipation in healthy subjects using a monetary incentive delay (MID) task by functional magnetic resonance imaging (fMRI), especially focusing on nucleus accumbens (NAc) activity to non-drug reward stimuli under bupropion treatment.
We used a randomized placebo-controlled within-subject crossover design. Fifteen healthy adults participated in two series of an fMRI study, taking either placebo or bupropion. The participants performed the MID task during the fMRI scanning. The effects of bupropion on behavioral performance and blood oxygenation level-dependent (BOLD) signal in NAc during anticipation of monetary gain were analyzed.
We found that bupropion significantly increased BOLD responses in NAc during monetary reward anticipation. The increased BOLD responses in NAc were observed with both low and high reward incentive cues. There was no significant difference between placebo and bupropion in behavioral performance.
Our findings provide support for the notion that bupropion enhances non-drug rewarding effects, suggesting a possible mechanism underlying therapeutic effects for patients with motivational deficit.
安非他酮用于治疗重度抑郁症、戒烟辅助和肥胖症。它可阻断多巴胺和去甲肾上腺素的再摄取，并拮抗烟碱型乙酰胆碱受体。动物研究表明，安非他酮可增强奖赏效应。此外，安非他酮具有治疗奖赏处理功能障碍患者的潜力。然而，人类受试者中安非他酮对奖赏功能影响的神经基础尚不完全清楚。
我们通过功能磁共振成像（fMRI）研究了单次给予安非他酮对健康受试者奖赏预期的神经反应的影响，使用的是金钱激励延迟（MID）任务，特别是关注安非他酮治疗下对非药物奖赏刺激的伏隔核（NAc）活动。
我们使用随机安慰剂对照、个体内交叉设计。15 名健康成年人参与了两项 fMRI 研究系列，分别服用安慰剂或安非他酮。参与者在 fMRI 扫描期间执行 MID 任务。分析了安非他酮对预期金钱收益时 NAc 中的行为表现和血氧水平依赖（BOLD）信号的影响。
我们发现，安非他酮可显著增加 NAc 在金钱奖赏预期期间的 BOLD 反应。在低和高奖赏线索下均观察到 NAc 中 BOLD 反应的增加。在行为表现方面，安慰剂和安非他酮之间没有显著差异。
我们的发现支持了安非他酮增强非药物奖赏效应的观点，这表明了治疗动机缺陷患者的潜在机制。
