Light provides the primary signal for entraining circadian rhythms to the day/night cycle. In addition to rods and cones, the retina contains a small population of photosensitive retinal ganglion cells (pRGCs) expressing the photopigment melanopsin (OPN4). Concerns have been raised that exposure to dim artificial lighting in the evening (DLE) may perturb circadian rhythms and sleep patterns, and OPN4 is presumed to mediate these effects. Here, we examine the effects of 4-h, 20-lux DLE on circadian physiology and behavior in mice and the role of OPN4 in these responses. We show that 2 wk of DLE induces a phase delay of ∼2 to 3 h in mice, comparable to that reported in humans. DLE-induced phase shifts are unaffected in Opn4^−/− mice, indicating that rods and cones are capable of driving these responses in the absence of melanopsin. DLE delays molecular clock rhythms in the heart, liver, adrenal gland, and dorsal hippocampus. It also reverses short-term recognition memory performance, which is associated with changes in preceding sleep history. In addition, DLE modifies patterns of hypothalamic and cortical cFos signals, a molecular correlate of recent neuronal activity. Together, our data show that DLE causes coordinated realignment of circadian rhythms, sleep patterns, and short-term memory process in mice. These effects are particularly relevant as DLE conditions―due to artificial light exposure―are experienced by the majority of the populace on a daily basis.

光提供了将昼夜节律引入昼夜循环的主要信号。除了视杆细胞和视锥细胞外，视网膜还包含一小群表达光色素黑视蛋白 (OPN4) 的光敏视网膜神经节细胞 (pRGC)。有人担心晚上暴露在昏暗的人工照明下 (DLE) 可能会扰乱昼夜节律和睡眠模式，并且推测 OPN4 可以调节这些影响。在这里，我们检查了 4 小时、20 勒克斯 DLE 对小鼠昼夜节律生理和行为的影响以及 OPN4 在这些反应中的作用。我们表明，2 周的 DLE 会在小鼠中诱导 2 到 3 小时的相位延迟，与人类报道的相近。DLE 引起的相移在Opn4中不受影响^-/-小鼠，表明视杆细胞和视锥细胞能够在没有黑视蛋白的情况下驱动这些反应。DLE 延迟心脏、肝脏、肾上腺和背侧海马的分子时钟节律。它还可以逆转与先前睡眠历史变化相关的短期识别记忆表现。此外，DLE 会改变下丘脑和皮质 cFos 信号的模式，这是与近期神经元活动相关的分子。总之，我们的数据表明，DLE 导致小鼠昼夜节律、睡眠模式和短期记忆过程的协调重新排列。这些影响尤其重要，因为大多数民众每天都会经历 DLE 条件（由于人工光照）。