Potent Circadian Effects of Dim Illumination at Night in Hamsters

Conventional wisdom holds that the circadian pacemaker of rodents and humans is minimally responsive to light of the intensity provided by dim moonlight and starlight. However, dim illumination (<0.005 lux) provided during the daily dark periods markedly alters entrainment in hamsters. Under dimly lit scotophases, compared to completely dark ones phases, the upper range of entrainment is increased by ～4 h, and re‐entrainment is accelerated following transfer from long to short day lengths. Moreover, the incidence of bimodal entrainment to 24 h light:dark:light:dark cycles is increased fourfold. Notably, the nocturnal illumination inducing these pronounced effects is equivalent in photic energy to that of a 2 sec, 100 lux light pulse. These effects may be parsimoniously interpreted as an action of dim light on the phase relations between multiple oscillators comprising the circadian pacemaker. An action of dim light distinct from that underlying bright‐light phase‐resetting may promote more effective entrainment. Together, the present results refute the view that scotopic illumination is environmental “noise” and indicate that clock function is conspicuously altered by nighttime illumination like that experienced under dim moonlight and starlight. We interpret our results as evidence for a novel action of dim light on the coupling of multiple circadian oscillators.     

Circadian Rhythm of Acute Phase Proteins under the Influence of Bright/Dim Light during the Daytime

We investigated the influence of two different light intensities, dim (100 lx) and bright (5,000 lx), during the daytime on the circadian rhythms of selected acute phase proteins of C‐reactive protein (CRP), α1‐acid glycoprotein (AGP), α1‐antichymotrypsin (ACT), transfferin (TF), α2‐macroglobulin (α2‐m), haptoglobin (HP), and ceruloplasmin (CP). Serum samples were collected from 7 healthy volunteers at 4 h intervals during two separate single 24 h spans during which they were exposed to the respective light intensity conditions. A circadian rhythm was detected only in ACT concentration in the bright light condition. The concentration of ACT, a positive acute phase protein (APP), increased (significantly significant differences in the ACT concentration were detected at 14:00 and 22:00 h) and AGP showed a tendency to be higher under the daytime bright compared to dim light conditions. There were no significant differences between the time point means under daytime dim and bright light conditions for α2‐M, AGP, Tf, Cp, or Hp. The findings suggest that some, but not all, APP may be influenced by the environmental light intensity.     

Calcium and Photoentrainment in Chick Pineal Cells Revisited: Effects of Caffeine, Thapsigargin, EGTA, and Light on the Melatonin Rhythm

Abstract: Chick pineal cells in dispersed cell culture display a persistent, photosensitive, circadian rhythm of melatonin production and release. Light pulses have at least two distinguishable effects on these cells, i.e., acute suppression of melatonin output and phase shifts (entrainment) of the underlying circadian pacemaker. Previous results linked calcium influx through voltage-sensitive calcium channels in the plasma membrane to acute regulation of melatonin synthesis but denied a role for such influx in entrainment. Those experiments did not, however, address the role of intracellular calcium metabolism. Here we describe the effects of pulses of caffeine, thapsigargin, and EGTA on the melatonin rhythm, and their interactions with the effects of light pulses. Caffeine had two distinguishable effects on these cells, acute enhancement of melatonin output (attributable to phosphodiesterase inhibition) and phase shifts of the circadian pacemaker with a light-like pattern (attributable to effects on intracellular calcium). Phase shifts induced by light and caffeine were not additive. Thapsigargin (which specifically blocks the pump that replenishes intracellular calcium stores, thereby increasing cytoplasmic calcium and depleting intracellular stores) had no phase-shifting effects by itself but reduced the size of the phase advances induced by caffeine or light. Low calcium solution acutely suppressed melatonin output without inducing phase shifts or affecting those induced by caffeine or light. However, addition of EGTA (which specifically chelates calcium, thereby lowering cytoplasmic calcium and depleting intracellular stores) did reduce the size of phase advances induced by caffeine or light, in normal medium or in low calcium solution, without inducing a phase shift by itself at that phase. Taken together, these results point toward a role for intracellular calcium fluxes in entrainment of the circadian pacemaker.     

Effects of Prolonged Exposure to Darkness on Circadian Photic Responsiveness in the Mouse

Circadian rhythms in mammals are generated by an endogenous pacemaker but are modulated by environmental cycles, principally the alternation of light and darkness. Although much is known about nonparametric effects of light on the circadian system, little is known about other effects of photic stimulation. In the present study, which consists of a series of five experiments in mice, various manipulations of photic stimulation were used to dissect the mechanisms responsible for a variation in the magnitude of light-induced phase-shifts that results from prolonged exposure to darkness. The results confirmed previous observations that prolonged exposure to darkness causes an increase in the magnitude of phase shifts (both phase advances and phase delays) evoked by discrete light pulses. The results also indicated that the increase in responsiveness results from the lack of exposure to light per se and not from collateral effects of exposure to constant darkness such as the lack of previous entrainment. The lack of exposure to light causes the circadian system to undergo a process of dark adaptation similar to dark adaptation in the visual system but with a much slower temporal course. The results suggest that circadian dark adaptation may take place at the retinal level, but it is not clear whether it involves a change in the sensitivity or maximal responsiveness of the system.     

Reconfiguration of a Multi-oscillator Network by Light in the Drosophila Circadian Clock

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Ontogeny of the Circadian System During Embryogenesis in Rainbow Trout (Oncorhynchus mykyss) and the Effect of Prolonged Exposure to Continuous Illumination on Daily Rhythms of per1, clock,and aanat2 Expression

It is widely held that the development of the circadian system during embryogenesis is important for future survival of an organism. Work in teleosts has been, to date, limited to zebrafish, which provides little insight into the diversity of this system within such a large vertebrate class. In this study, the authors analyzed the diel expression of per1, clock, and aanat2 in unfertilized rainbow trout oocytes and embryos maintained under either a 12:12-h light:dark (LD) cycle or continuous illumination (LL) from fertilization. 24-h profiles in expression were measured at fertilization as well as 8, 21 42, and 57 days postfertilization (dpf). Both per1 and clock were expressed in unfertilized oocytes and all embryonic stages, whereas aanat2 expression was only measureable from 8 dpf. A reduction in both per1 and clock mean expression levels between unfertilized oocytes/0–1 dpf embryos and 8–9 dpf embryos was suggestive of a transition from maternal RNA to endogenous mRNA expression. Although aanat2 expression was not clearly associated with photic conditions, photoperiod treatment did alter the expression of per1 and clock expression/rhythmicity from as early as 8 dpf (per1), which could suggest the presence and functionality of an as yet unidentified “photoreceptor.” As a whole, this work demonstrates that clock systems are present and functional during embryonic development in rainbow trout. Further studies of their expression and regulation will help understand how the environment interacts with embryonic development in the species. (Author correspondence: andrew.davie@stir.ac.uk)