Abstract:Non-technical summary The human biological clock organizes and regulates the timing of many biochemical and physiological processes, including the timing of sleep, on a daily basis. Light is the strongest time cue to the circadian clock that keeps these rhythms entrained to the 24 h day. Light exposure at night results in 'resetting' of the clock (phase shifting). In the current study, we examined the effects of exposing subjects to two different light levels (very dim light vs. typical room light) before expo… Show more
“…In the current analyses, we assessed phase shifts over three cycles, consistent with previous studies (21-23); however, the endogenous drift over multiple circadian cycles between assessments may influence the phase shift results compared with results calculated across only one or two circadian cycles (22,24,25). Additionally, the studies were performed against a dim light background, which reduces the masking effects of light on the circadian pacemaker but can cause moderate sensitization of the system to subsequent bright LEs (26,27). Although the mean illuminances appeared to differ between the duration conditions with up to a ~45% difference between the highest mean (9,040 lux, 1 hour condition) and lowest mean intensities (6,226 lux, 2 minute condition), it is highly unlikely that this affected the phase resetting responses.…”
IntroductionLight is the strongest environmental time cue for resetting the circadian clock in mammals, including humans (1, 2). Initial studies examining the phase-resetting effects of light used long-duration (5 hours) and high-intensity (~9,500 lux) light (2) because the human circadian system was thought to be less sensitive to light than that of other mammals. While the circadian pacemaker in mice (3), rats (4), hamsters (5), and humans (6, 7) is known to respond to a sequence of millisecond flashes (administered over 5 seconds in rats, over 5-60 minutes in mice and hamsters, and over 60 minutes in humans), a single millisecond flash does not reset the mammalian pacemaker at the intensities that have been tested (3,8), suggesting that circadian resetting requires integration of the photic signal over a longer exposure interval.A nonlinear relationship exists between light exposure (LE) duration and the magnitude of circadian phase resetting responses. A single 12-minute pulse of light can shift the human pacemaker 8 times more BACKGROUND. In humans, a single light exposure of 12 minutes and multiple-millisecond light exposures can shift the phase of the circadian pacemaker. We investigated the response of the human circadian pacemaker to a single 15-second or 2-minute light pulse administered during the biological night.
“…In the current analyses, we assessed phase shifts over three cycles, consistent with previous studies (21-23); however, the endogenous drift over multiple circadian cycles between assessments may influence the phase shift results compared with results calculated across only one or two circadian cycles (22,24,25). Additionally, the studies were performed against a dim light background, which reduces the masking effects of light on the circadian pacemaker but can cause moderate sensitization of the system to subsequent bright LEs (26,27). Although the mean illuminances appeared to differ between the duration conditions with up to a ~45% difference between the highest mean (9,040 lux, 1 hour condition) and lowest mean intensities (6,226 lux, 2 minute condition), it is highly unlikely that this affected the phase resetting responses.…”
IntroductionLight is the strongest environmental time cue for resetting the circadian clock in mammals, including humans (1, 2). Initial studies examining the phase-resetting effects of light used long-duration (5 hours) and high-intensity (~9,500 lux) light (2) because the human circadian system was thought to be less sensitive to light than that of other mammals. While the circadian pacemaker in mice (3), rats (4), hamsters (5), and humans (6, 7) is known to respond to a sequence of millisecond flashes (administered over 5 seconds in rats, over 5-60 minutes in mice and hamsters, and over 60 minutes in humans), a single millisecond flash does not reset the mammalian pacemaker at the intensities that have been tested (3,8), suggesting that circadian resetting requires integration of the photic signal over a longer exposure interval.A nonlinear relationship exists between light exposure (LE) duration and the magnitude of circadian phase resetting responses. A single 12-minute pulse of light can shift the human pacemaker 8 times more BACKGROUND. In humans, a single light exposure of 12 minutes and multiple-millisecond light exposures can shift the phase of the circadian pacemaker. We investigated the response of the human circadian pacemaker to a single 15-second or 2-minute light pulse administered during the biological night.
“…In experiments with human subjects, the circadian system was found to be adaptive and maintain a high plasticity, as prior exposure to dim light was shown to influence MLT suppression following more intensive light stimuli (Jasser et al, 2006;Chang et al, 2011). According to our results, long AD causes the decrease in response in regard to hsp70 expression and protein levels, probably because the animal becomes used to the LI.…”
SUMMARYLight at night and light interference (LI) disrupt the natural light:dark cycle, causing alterations at physiological and molecular levels, partly by suppressing melatonin (MLT) secretion at night. Heat shock proteins (HSPs) can be activated in response to environmental changes. We assessed changes in gene expression and protein level of HSP70 in brain and hepatic tissues of golden spiny mice (Acomys russatus) acclimated to LI for two (SLI), seven (MLI) and 21 nights (LLI). The effect of MLT treatment on LI-mice was also assessed. HSP70 levels increased in brain and hepatic tissues after SLI, whereas after MLI and LLI, HSP70 decreased to control levels. Changes in HSP70 levels as a response to MLT occurred after SLI only in hepatic tissue. However, hsp70 expression following SLI increased in brain tissue, but not in hepatic tissue. MLT treatment and SLI caused a decrease in hsp70 levels in brain tissue and an increase in hsp70 in hepatic tissue. SLI acclimation elicited a stress response in A. russatus, as expressed by increased HSP70 levels and gene expression. Longer acclimation decreases protein and gene expression to their control levels. We conclude that for brain and hepatic tissues of A. russatus, LI is a short-term stressor. Our results also revealed that A. russatus can acclimate to LI, possibly because of its circadian system plasticity, which allows it to behave both as a nocturnal and as a diurnal rodent. To the best of our knowledge, this is the first study showing the effect of LI as a stressor at the cellular level, by activating HSP70.
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“…For instance, an increased sensitivity to light may develop with age to compensate for chronic exposure to lower levels of light due to lens opacification. Several studies in young individuals have shown that, following prolonged exposure to low light levels, exposure to light induces stronger suppression and phase shift of melatonin secretion (Chang et al, 2011;Hebert et al, 2002;Jasser et al, 2006). An alternative explanation for the smaller pupil size in the elderly, despite the lack of a difference in relative pupil constriction, is a loss of tonic control of pupil dilation, previously suggested in a study of nonhuman primates (Clarke et al, 2003).…”
Many nonvisual functions are regulated by light through a photoreceptive system involving melanopsin-expressing retinal ganglion cells that are maximally sensitive to blue light. Several studies have suggested that the ability of light to modulate circadian entrainment and to induce acute effects on melatonin secretion, subjective alertness, and gene expression decreases during aging, particularly for blue light. This could contribute to the documented changes in sleep and circadian regulatory processes with aging. However, age-related modification in the impact of light on steady-state pupil constriction, which regulates the amount of light reaching the retina, is not demonstrated. We measured pupil size in 16 young (22.8 ± 4 years) and 14 older (61 ± 4.4 years) healthy subjects during 45-second exposures to blue (480 nm) and green (550 nm) monochromatic lights at low (7 à 1012 photons/cm2/s), medium (3 à 1013 photons/cm2/s), and high (1014 photons/cm2/s) irradiance levels. Results showed that young subjects had consistently larger pupils than older subjects for dark adaptation and during all light exposures. Steady-state pupil constriction was greater under blue than green light exposure in both age groups and increased with increasing irradiance. Surprisingly, when expressed in relation to baseline pupil size, no significant age-related differences were observed in pupil constriction. The observed reduction in pupil size in older individuals, both in darkness and during light exposure, may reduce retinal illumination and consequently affect nonvisual responses to light. The absence of a significant difference between age groups for relative steady-state pupil constriction suggests that other factors such as tonic, sympathetic control of pupil dilation, rather than light sensitivity per se, account for the observed age difference in pupil size regulation. Compared to other nonvisual functions, the light sensitivity of steady-state pupil constriction appears to remain relatively intact and is not profoundly altered by age.
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