A link between dopamine levels, circadian gene expression, and attention deficit hyperactivity disorder (ADHD) has already been demonstrated. The aim of this study was to investigate the extent of these relationships by measuring circadian gene expression in primary human-derived dermal fibroblast cultures (HDF) after dopamine exposure. We analyzed circadian preference, behavioral circadian and sleep parameters as well as the circadian gene expression in a cohort of healthy controls and participants with ADHD. Circadian preference was evaluated with German Morningness-Eveningness-Questionnaire (D-MEQ) and rhythms of sleep/wake behavior were assessed via actigraphy. After ex vivo exposure to different dopamine concentrations in human dermal fibroblast (HDF) cultures, the rhythmicity of circadian gene expression (Clock, Bmal1, Per1-3, Cry1) was analyzed via qRT-PCR. We found no statistical significant effect in the actigraphy of both groups (healthy controls, ADHD group) for mid-sleep on weekend days, mid-sleep on weekdays, social jetlag, wake after sleep onset, and total number of wake bouts. D-MEQ scores indicated that healthy controls had no evening preference, whereas subjects with ADHD displayed both definitive and moderate evening preferences. Dopamine has no effect on Per3 expression in healthy controls, but produces a significant difference in the ADHD group at ZT24 and ZT28. In the ADHD group, incubation with dopamine, either 1 µM or 10 µM, resulted in an adjustment of Per3 expression to control levels. A similar effect also was found in the expression of Per2. Statistical significant differences in the expression of Per2 (ZT4) in the control group compared to the ADHD group were found, following incubation with dopamine. The present study illustrates that dopamine impacts on circadian function. The results lead to the suggestion that dopamine may improve the sleep quality as well as ADHD symptoms by adjustment of the circadian gene expression, especially for Per2 and Per3.

多巴胺水平、昼夜节律基因表达和注意力缺陷多动障碍 (ADHD) 之间的联系已经得到证实。本研究的目的是通过测量多巴胺暴露后原代人源性真皮成纤维细胞培养 (HDF) 中的昼夜节律基因表达来研究这些关系的程度。我们分析了一组健康对照和 ADHD 参与者的昼夜节律偏好、行为昼夜节律和睡眠参数以及昼夜节律基因表达。昼夜节律偏好通过德国晨昏-晚上问卷 (D-MEQ) 进行评估，睡眠/清醒行为的节律通过活动记录仪进行评估。离体后在人类真皮成纤维细胞 (HDF) 培养物中暴露于不同的多巴胺浓度，通过 qRT-PCR 分析昼夜节律基因表达 ( Clock、Bmal1、Per1-3、Cry1 ) 的节律性。我们发现两组（健康对照组、ADHD 组）在周末睡眠中、工作日中睡眠、社交时差、入睡后醒来和醒来总次数的活动记录中没有显着影响。D-MEQ 评分表明健康对照组没有晚间偏好，而患有 ADHD 的受试者则表现出明确和中度的晚间偏好。多巴胺对Per3没有影响在健康对照中表达，但在 ZT24 和 ZT28 的 ADHD 组中产生显着差异。在 ADHD 组中，与 1 μM 或 10 μM 的多巴胺孵育导致Per3表达调整到控制水平。在Per2的表达中也发现了类似的效果。与多巴胺孵育后，发现对照组与 ADHD 组相比， Per2 (ZT4)的表达存在统计学显着差异。本研究表明多巴胺对昼夜节律功能的影响。结果表明，多巴胺可以通过调整昼夜节律基因表达来改善睡眠质量和 ADHD 症状，尤其是Per2和Per3。