How light at night resets the melatonin rhythm
The pineal gland releases melatonin at night, and this nightly signal is controlled by the suprachiasmatic nuclei (SCN), a small cluster of neurons in the hypothalamus that acts as the body's master clock [1]. When light hits the eye at night, it reaches the SCN and can reset the timing of the melatonin rhythm. Research on mammals has shown that both short light pulses and long exposures to light at night can reset this rhythm, but the two produce different effects on the clock [1].
In humans, a systematic review of light exposure studies found that melatonin secretion is sensitive to light timing and duration, with even intermittent light exposures and long-wavelength red light capable of influencing melatonin levels [2]. This means the resetting effect is not limited to bright white light or continuous exposure; the pattern of light delivery matters.
Short pulses shift timing; long exposures compress the signal
A short pulse of light at night acts like a timing cue: it can shift the phase of the melatonin rhythm, moving the nightly melatonin window earlier or later depending on when the pulse arrives [1]. This is the kind of resetting that helps an animal adjust its internal clock to a new light-dark schedule, such as after travel or a seasonal change in sunrise time.
A long exposure to light at night works differently. Instead of just shifting the rhythm, it can truncate the melatonin signal by suppressing melatonin production for as long as the light is on [1]. The result is a shorter nightly melatonin peak. In this way, the duration of the melatonin signal becomes a direct reflection of the length of the dark period.
Why the melatonin signal works as a calendar
The SCN uses the melatonin rhythm not just to organize daily sleep and wake cycles but also to measure the time of year [1]. Because the length of the nocturnal melatonin signal tracks the length of the night, a long melatonin signal indicates a long night (winter), while a short signal indicates a short night (summer). This is how the brain can encode day length and adjust seasonal physiology.
The key insight from decades of chronobiology research is that the SCN itself changes its functional properties depending on photoperiod, meaning the central clock is not just a daily timekeeper but also a seasonal calendar [1]. Long light exposures at night alter the melatonin signal's duration, and that duration is what the brain reads as a measure of day length.
What is less clear in humans
Most of the detailed mechanistic evidence for how light resets the melatonin rhythm and encodes day length comes from animal studies [1]. In humans, the picture is consistent but less complete: light exposure clearly affects melatonin secretion and can shift circadian timing [2], and studies of dim light melatonin onset show that morning or evening light can shift the timing of melatonin release [3]. However, how precisely these shifts translate into day-length encoding in people is not directly established by the available evidence.
Sources used in this answer
From the Pineal Gland to the Central Clock in the Brain: Beginning of Studies of the Mammalian Biological Rhythms in the Institute of Physiology of the Czech Academy of Sciences
Reviews research showing that short light pulses and long light exposures at night reset the pineal melatonin rhythm through different mechanisms, and that photoperiod modulates SCN function so the clock can serve as a seasonal calendar.
Systematic review of light exposure impact on human circadian rhythm
A systematic review found that various light exposures, including intermittent pulses and long wavelengths, can influence human melatonin secretion and circadian resetting.
Effects of light exposure and sleep displacement on dim light melatonin onset
Three days of morning or evening light exposure shifted dim light melatonin onset, indicating that light timing can reset the pineal melatonin rhythm in humans.