Two Coupled Circadian Oscillators Are Involved in Nonphotic Acceleration of Reentrainment to Shifted Light Cycles in Mice (original) (raw)
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Genes to Cells, 2008
Effects of scheduled exposures to novel environment with a running-wheel were examined on re-entrainment to 8 hour shifted light-dark (LD) cycles of mouse circadian rhythms in locomotor activity and clock gene, Per1, expression in the suprachiasmatic nucleus (SCN) and peripheral tissues. Per1 expression was monitored by a bioluminescence reporter introduced into mice. The animals were exposed to the novel environment for 3 hours from the shifted dark onset for 4 cycles and released into constant darkness. In the phase-advance shift, the circadian rhythm in locomotor activity fully re-entrained in the exposed group, whereas it was in transients in the control. On the other hand, the circadian rhythm of Per1 expression in the SCN almost completely re-entrained in both the control and exposed groups. In the skeletal muscle and lung, the circadian rhythm fully re-entrained in the exposed group, whereas the rhythms in the control did not. In the phase-delay shift, the circadian rhythms in locomotor activity and Per1 expression almost completely re-entrained in both groups. Theses findings indicate that the scheduled exposures to novel environment with a running-wheel differentially accelerate the re-entrainment of the mouse peripheral clocks to 8 hour phase-advanced LD cycles.
Extraordinary behavioral entrainment following circadian rhythm bifurcation in mice
The mammalian circadian timing system uses light to synchronize endogenously generated rhythms with the environmental day. Entrainment to schedules that deviate significantly from 24 h (T24) has been viewed as unlikely because the circadian pacemaker appears capable only of small, incremental responses to brief light exposures. Challenging this view, we demonstrate that simple manipulations of light alone induce extreme plasticity in the circadian system of mice. Firstly, exposure to dim nocturnal illumination (<0.1 lux), rather than completely dark nights, permits expression of an altered circadian waveform wherein mice in light/dark/light/dark (LDLD) cycles " bifurcate " their rhythms into two rest and activity intervals per 24 h. Secondly, this bifurcated state enables mice to adopt stable activity rhythms under 15 or 30 h days (LDLD T15/T30), well beyond conventional limits of entrainment. Continuation of dim light is unnecessary for T15/30 behavioral entrainment following bifurcation. Finally, neither dim light alone nor a shortened night is sufficient for the extraordinary entrainment observed under bifurcation. Thus, we demonstrate in a non-pharmacological, non-genetic manipulation that the circadian system is far more flexible than previously thought. These findings challenge the current conception of entrainment and its underlying principles, and reveal new potential targets for circadian interventions.
European Journal of Neuroscience, 2004
Behavioral (nonphotic) stimuli can shift circadian rhythms by serotonin (5-HT) and/or neuropeptide Y (NPY) inputs to the suprachiasmatic nucleus (SCN) circadian clock. Based on the idea that behavioral phase resetting is modulated by endogenous changes in postsynaptic sensitivity to such transmitters, hamsters were exposed to constant light (LL; $ 250 lx) for 1±3 days, which suppresses locomotor activity and eliminates the daily rhythm of SCN 5-HT release measured by microdialysis. Groups subjected to brief LL or maintained under a light/dark cycle (LD) received phase-resetting treatments with the 5-HT 1A,7 agonist (AE)-2-dipropyl-amino-8hydroxyl-1,2,3,4-tetrahydronapthalene (8-OH-DPAT) or sleep deprivation (SD). Animals were released to constant darkness at the start of the treatments. Phase advances to 8-OH-DPAT and SD during the day were 11 and 3 h for LL vs. 2 and 1 h for LD, respectively. Phase delays during the night were À12 and À5 h for LL vs. no responses for LD, respectively. Phase-transition curves for both LL treatments had slopes approximating 0, indicative of Type 0 phase resetting. For all treatments, the degree of locomotor suppression by LL was not correlated with the phase shift magnitude. Re-establishing locomotor activity by overnight food deprivation did not prevent potentiated shifting to SD. However, re-establishing peak extracellular 5-HT levels by intra-SCN 5-HT reverse microdialysis perfusion in LL did signi®cantly reduce potentiated 8-OH-DPAT phase advances. Constant light also enhanced intra-SCN NPY-induced phase advances during the day (6 vs. 2 h for LD). These results suggest that LL promotes Type 0 phase resetting by supersensitizing 5-HT and/or NPY postsynaptic responses and possibly by attenuating the amplitude of the circadian pacemaker, thus enhancing circadian clock resetting nonspeci®cally.
Circadian system of mice integrates brief light stimuli
The American journal of physiology, 1998
Light is the primary sensory stimulus that synchronizes or entrains the internal circadian rhythms of animals to the solar day. In mammals photic entrainment of the circadian pacemaker residing in the suprachiasmatic nuclei is due to the fact that light at certain times of day can phase shift the pacemaker. In this study we show that the circadian system of mice can integrate extremely brief, repeated photic stimuli to produce large phase shifts. A train of 2-ms light pulses delivered as one pulse every 5 or 60 s, with a total light duration of 120 ms, can cause phase shifts of several hours that endure for weeks. Single 2-ms pulses of light were ineffective. Thus these data reveal a property of the mammalian circadian clock: it can integrate and store latent sensory information in such a way that a series of extremely brief photic stimuli, each too small to cause a phase shift individually, together can cause a large and long-lasting change in behavior.
Neuroscience Research, 1992
Adjustment of the circadian clock to shifts in the light/dark (LD) cycle was assessed from the rat pineal N-acetyltransferase (NAT) rhythm which is controlled by a pacemaker in the suprachiasmatic nucleus of the hypothalamus. Re-entrainment to an 8-h delay in the LD cycle took more than 3 days in rats maintained under a regime with 18 h of light and 6 h of darkness per day (LD 18:6) whereas it was completed within 3 days in those maintained under LD 12: 12. Re-entrainment to an advance in the LD cycle proceeded through a transient diminution or almost disappearance of the NAT rhythm amplitude following a 5-h, 3-h and even a mere 2-h advance shift under LD 18:6, whereas no such diminution occurred under LD 12:12 even after a 5-h advance shift. Altogether, the data indicate that resetting of the circadian clock after shifts in the LD cycle depends on the photoperiod. In a non-periodic environment, the mammalian circadian clock freeruns with a period close to, but not equal to, 24 h I. Under natural daylight or in a 24-h artificial light/dark (LD) cycle, the clock is synchronized to the 24-h day by periodic changes in light and darkness Is. Following shifts in the LD cycle which mimic transmeridian flights, the circadian pacemaker must readjust to a new environmental time. In previous papers we studied re-entrainment of the clock after shifts in the LD cycle in rats maintained under only one photoperiod, namely in a regime with 12 h of light and 12 h of darkness per day (LD 12 : 12) 4'6'7'12. As recent data suggest that resetting of the circadian pacemaker may depend on the photoperiod s'9, we decided to study re-entrainment of the clock after shifts in the LD cycle in rats maintained under another photoperiod, this time under a longer one, in order to compare the readjustment under different photoperiods. To assess the phases of the circadian pacemaker, we used the overt rhythm in pineal N-acetyltransferase (NAT) (arylalkylamine: acetyl CoA N-acetyltransferase, EC 2.3.1.87) activity which drives rhythmic melatonin production in the rat 11"15, as hands of the clock. The NAT rhythm is controlled by a pacemaker located in the suprachiasmatic nuclei of the hypothalamus 14, as are other circadian rhythms 16,2°. At night, according to the
Scientific Reports
Circadian rhythms are regulated by molecular clockwork and drive 24-h behaviors such as locomotor activity, which can be rendered non-functional through genetic knockouts of clock genes. Circadian rhythms are robust in constant darkness (DD) but are modulated to become exactly 24 h by the external day-night cycle. Whether ill-timed light and dark exposure can render circadian behaviors non-functional to the extent of genetic knockouts is less clear. In this study, we discovered an environmental approach that led to a reduction or lack in rhythmic 24-h-circadian wheel-running locomotor behavior in mice (referred to as arrhythmicity). We first observed behavioral circadian arrhythmicity when mice were gradually exposed to a previously published disruptive environment called the fragmented day-night cycle (FDN-G), while maintaining activity alignment with the four dispersed fragments of darkness. Remarkably, upon exposure to constant darkness (DD) or constant light (LL), FDN-G mice los...
Journal of Biological Rhythms, 2006
In nature, virtually all circadian rhythms assume the 24.0-h period of the solar day-night cycle. This is due to the entrainment of the endogenous oscillators to the external light-dark cycle, the dominant zeitgeber for the majority of organisms. The process of entrainment is based on differential phase and period responses of the circadian systems to light depending on the phase at which the stimulus is applied. The