Phase-Shifting Effects of Light and Activity on the Human Circadian Clock

1994 ◽  
Author(s):  
Eve Van Cauter
1993 ◽  
Author(s):  
Eve Van Cauter ◽  
Jeppe Sturis ◽  
Maria M. Byrne ◽  
John D. Blackman ◽  
Neal H. Scherberg ◽  
...  

1990 ◽  
Vol 5 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Carl Hirschie Johnson ◽  
Hideaki Nakashima

1986 ◽  
Vol 250 (1) ◽  
pp. R5-R17
Author(s):  
D. P. Lotshaw ◽  
J. W. Jacklet

The effects of the protein synthesis inhibitors anisomycin and puromycin were measured on protein synthesis and phase shifting of the circadian rhythm in the isolated Aplysia eye. Anisomycin pulses induce phase delays proportional in magnitude to the duration and percentage of protein synthesis inhibition. The phase-response curve to anisomycin pulses consisted of delays induced throughout the subjective night. Delays were maximal between circadian times (CT) 18 and CT 2; pulses initiated between CT 2 and CT 12 did not phase shift. Puromycin induced phase delays and advances. Delays were proportional to the duration and percentage of protein synthesis inhibition, occurring with increasing magnitude throughout the subjective night (CT 12-2). Peptidyl-puromycin formation may contribute to the magnitude of the delay. Advances, occurring between CT 2 and CT 8, required a greater drug concentration and pulse duration than delays and appeared to result from an effect other than protein synthesis inhibition. Our results support the hypothesis of a phase-dependent requirement for protein synthesis during the subjective night in this circadian clock.


1998 ◽  
Vol 275 (2) ◽  
pp. E243-E248 ◽  
Author(s):  
Bernard Goichot ◽  
Laurence Weibel ◽  
Florian Chapotot ◽  
Claude Gronfier ◽  
François Piquard ◽  
...  

To determine the effect of a phase shift in sleep on the circadian clock, thyroid-stimulating hormone (TSH), cortisol, and melatonin, three robust markers of the circadian clock, were analyzed using a 10-min blood sampling procedure. In an initial experiment eight subjects were studied during two experimental sessions: once under baseline conditions with normal nighttime sleep from 2300 to 0700 (baseline) and once after a night of sleep deprivation followed by daytime sleep from 0700 to 1500 ( day 1). In a second experiment, carried out on seven subjects, the 24-h hormone profiles of the first day ( day 1) were compared with those of the second day ( day 2) of the sleep shift. During the night of sleep deprivation ( day 1) the TSH surge was higher than during baseline conditions, whereas melatonin and cortisol rhythms remained unaffected. On day 2 the amplitude of the nocturnal TSH surge was reduced in comparison to day 1, whereas the amplitudes of melatonin and cortisol rhythms were unchanged. There was a clear phase shift in the three endocrine rhythms. Triiodothyronine levels were slightly higher in the morning after the first night of sleep deprivation. These results demonstrate that 2 consecutive days of sleep shift are sufficient to affect the timing of the commonly accepted circadian markers, suggesting the existence of a rapid resetting effect on the circadian clock. TSH reacts in a distinctive manner to the sleep-wake cycle manipulation by modulating the amplitude of the nocturnal surge. This amplitude modulation is probably an integral part of the phase-shifting mechanisms controlled by the circadian clock.


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