Circadian Entrainment to Temperature, But Not Light, in the Isolated  Suprachiasmatic Nucleus

Herzog, Erik D.; Huckfeldt, Rachel M.

doi:10.1152/jn.00129.2003

Cited by 76 publications

(67 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

supporting

confidence: 92%

“…3). The phase shift induced by changing the ambient temperature in our experiments is consistent with a previous study that demonstrated that the SCN entrains to temperature cycles (Herzog and Huckfeldt, 2003).In summary, our results demonstrate that the periods of mammalian peripheral tissues are temperature compensated over the range of 29 to 37 °C. We find tissuespecific differences in the Q 10 and in temperature-induced shifts of circadian phase.…”

supporting

confidence: 92%

See 1 more Smart Citation

Mammalian Peripheral Circadian Oscillators Are Temperature Compensated

2008

View full text Add to dashboard Cite

Variations in ambient temperature present a unique obstacle to the timekeeping function of circadian clocks. Most biological reactions proceed with a temperature coefficient (Q 10 ) ∼ 2 or 3, so that with every 10 °C increase in temperature, the reaction rate approximately doubles or triples. Therefore, a temperature-dependent clock would run faster at high temperatures than at low temperatures, and would not be a reliable predictor of time of day. So it is not surprising that mechanisms have evolved to ensure that the length of the circadian period remains relatively constant over a wide range of temperatures, a phenomenon known as temperature compensation.In mammals, self-sustaining rhythms have been measured in the master circadian clock, located in the SCN, and in peripheral tissues in vitro (Yamazaki et al., 2000;Yoo et al., 2004). When separated from the entrainment of the SCN, each peripheral tissue expresses tissue-specific differences in circadian period and phase (Yoo et al., 2004). While previous studies have shown that the circadian period in the SCN, retina, and in fibroblast cell lines remains relatively constant across a range of temperatures, it is unknown whether mammalian peripheral clocks are temperature compensated (Tosini and Menaker, 1998;Ruby et al., 1999;Izumo et al., 2003;Tsuchiya et al., 2003).To examine the effect of temperature on circadian oscillations, we measured PERIOD2::LUCIFERASE (PER2::LUC) rhythms in explants of central and peripheral tissues from mPer2 Luc mice at 29, 31, 33, 35, and 37 °C. At temperatures ranging from 31 to 37 °C, robust rhythms of PER2::LUC were measured in the SCN, pituitary gland, cornea, adrenal gland, and lung. In the liver, the rhythm of PER2::LUC was robust at 37 °C, but damped within 2 cycles at all other temperatures examined. At 29 °C, only the pituitary consistently maintained a robust PER2::LUC rhythm.To determine if circadian clocks in mammalian central and peripheral tissues were temperature compensated, we calculated the average period of each tissue at various temperatures. The Q 10 of the SCN, pituitary gland, cornea, adrenal gland, and lung were variable, but all were close to 1, suggesting that these tissues were temperature compensated (Fig. 1). Because the PER2::LUC rhythm of liver explants was not robust at temperatures below 37 °C, the Q 10 of the liver could not be calculated. Since Per2 participates in the transcriptional/translational feedback loops that regulate the expression of other circadian genes, temperature-induced changes in the bioluminescent waveform of PER2::LUC expression could reflect variable processing of the components of the feedback loops. However, we found no differences in the waveforms of PER2::LUC expression between tissues cultured at 31 and 37 °C (Fig. 2). It is possible that the effects of temperature on the molecular mechanism of the clock are not reflected in rhythmic PER2::LUC expression and other circadian genes should also be assessed. Alternatively, our method may not be sensitive enough to detect tem...

show abstract

supporting

confidence: 92%

supporting

confidence: 92%

Mammalian Peripheral Circadian Oscillators Are Temperature Compensated

2008

View full text Add to dashboard Cite

show abstract

“…Nonetheless, it should be noted that the resilience of the SCN to temperature changes is somewhat controversial. Herzog and Huckfeldt (2003) reported that in vitro cultured SCN preparations from rats synchronized readily to 24-h temperature cycles. Ruby (2011) suggested that different explant sizes and culture conditions may account for the somewhat incoherent observations made in studies with SCN tissue.…”

Section: Body Temperature Rhythms As Zeitgebers For Peripheral Circadmentioning

confidence: 99%

“…Yet, the cellular clocks tick at approximately the same rate at different ambient temperatures and, in mammals, even at a slightly higher pace when temperature is decreasing (Izumo et al 2003;Tsuchiya et al 2003;Dibner et al 2009). In spite of the resilience of the circadian period length over physiologically occurring temperature ranges, temperature oscillations have been demonstrated to act as strong Zeitgebers in multiple species from unicellular organisms to mammals (Zimmerman et al 1968;Francis and Sargent 1979;Underwood and Calaban 1987;Brown et al 2002;Herzog and Huckfeldt 2003;Boothroyd et al 2007).…”

mentioning

confidence: 99%

Simulated body temperature rhythms reveal the phase-shifting behavior and plasticity of mammalian circadian oscillators

Saini

Morf²,

Stratmann³

et al. 2012

Genes Dev.

225

189

View full text Add to dashboard Cite

The circadian pacemaker in the suprachiasmatic nuclei (SCN) of the hypothalamus maintains phase coherence in peripheral cells through metabolic, neuronal, and humoral signaling pathways. Here, we investigated the role of daily body temperature fluctuations as possible systemic cues in the resetting of peripheral oscillators. Using precise temperature devices in conjunction with real-time monitoring of the bioluminescence produced by circadian luciferase reporter genes, we showed that simulated body temperature cycles of mice and even humans, with daily temperature differences of only 3°C and 1°C, respectively, could gradually synchronize circadian gene expression in cultured fibroblasts. The time required for establishing the new steady-state phase depended on the reporter gene, but after a few days, the expression of each gene oscillated with a precise phase relative to that of the temperature cycles. Smooth temperature oscillations with a very small amplitude could synchronize fibroblast clocks over a wide temperature range, and such temperature rhythms were also capable of entraining gene expression cycles to periods significantly longer or shorter than 24 h. As revealed by genetic loss-of-function experiments, heat-shock factor 1 (HSF1), but not HSF2, was required for the efficient synchronization of fibroblast oscillators to simulated body temperature cycles.[Keywords: circadian gene expression; body temperature rhythms; heat-shock factor 1 (HSF1); heat-shock factor 2 (HSF2)]

show abstract

“…One obvious change associated with general anesthesia is transient hypothermia. Changes in temperature can phaseshift circadian neuronal rhythms of suprachiasmatic nuclei maintained in vitro (Herzog and Huckfeldt, 2003;Ruby et al, 1999), raising the possibility that anesthesia-induced hypothermia plays an active role in the observed phaseshifts. Notably, hypothermia reached the lowest (absolute) values after propofol perfusion at the sleep/wake transition (ie at circadian time 10), the same time as propofol treatment induced subsequent phase-advances (Figures 3 and 5).…”

Section: Chronobiotic Effects Of Propofol Anesthesiamentioning

confidence: 99%

Reciprocal Relationships between General (Propofol) Anesthesia and Circadian Time in Rats

Challet

Gourmelen

Pévet

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Several common postdischarge symptoms, such as sleep disorders, headache, drowsiness or general malaise, evoke disturbances of circadian rhythms due to jet lag (ie crossing time zones) or shift work rotation. Considering that general anesthesia is associated with numerous effects on the central nervous system, we hypothesized that it may also act on the circadian timing system. We first determined the effects of the circadian timing on general anesthesia. We observed that identical doses of propofol showed marked circadian fluctuations in duration of effects, with a peak at the middle of the resting period (ie 7 h after lights on). Then, we examined the effects of general anesthesia on circadian timing, by analysing stable free-running circadian rhythms (ie in constant environmental conditions), an experimental approach used widely in circadian biology. Free-running rats were housed in constant darkness and temperature to assess possible phase-shifting effects of propofol anesthesia according to the time of the day. When administered around (72 h) the daily rest/activity transition point, a 30-min propofol anesthesia induced a 1-h phase advance in the free-running rest-activity rhythm, while anesthesia had no significant resetting effect at other times of the day. Anesthesia-induced hypothermia was not correlated with the phase-shifting effects of propofol anesthesia. From our results, anesthesia itself can reset circadian timing, and acts as a synchronizing cue for the circadian clock. Neuropsychopharmacology (2007) 32, 728-735.

show abstract

Circadian Entrainment to Temperature, But Not Light, in the Isolated Suprachiasmatic Nucleus

Cited by 76 publications

References 72 publications

Mammalian Peripheral Circadian Oscillators Are Temperature Compensated

Mammalian Peripheral Circadian Oscillators Are Temperature Compensated

Simulated body temperature rhythms reveal the phase-shifting behavior and plasticity of mammalian circadian oscillators

Reciprocal Relationships between General (Propofol) Anesthesia and Circadian Time in Rats

Contact Info

Product

Resources

About