Dim light in the evening causes coordinated realignment of circadian rhythms, sleep, and short-term memory

Significance In modern societies, people are regularly exposed to artificial light (e.g., light-emitting electronic devices). Dim light in the evening (DLE) imposes an artificial extension of the solar day, increasing our alertness before bedtime, delaying melatonin timing and sleep onset, and increasing sleepiness in the next morning. Using laboratory mice as a model organism, we show that 2 wk of 4-h, 20-lux DLE postpones rest–activity rhythms, delays molecular rhythms in the brain and body, and reverses the diurnal pattern of short-term memory performance. These results highlight the biological impact of DLE and emphasize the need to optimize our evening light exposure if we are to avoid shifting our biological clocks.
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.