scholarly journals Phase Shifts in the Circadian Rhythm in Plasma Concentrations of Melatonin in Rams Induced by a 1-Hour Light Pulse

1990 ◽  
Vol 5 (2) ◽  
pp. 97-106 ◽  
Author(s):  
K.-I. Maeda ◽  
G.A. Lincoln
2016 ◽  
Vol 310 (8) ◽  
pp. R759-R765 ◽  
Author(s):  
Helen J. Burgess ◽  
Muneer Rizvydeen ◽  
Louis F. Fogg ◽  
Ali Keshavarzian

Central circadian timing influences mental and physical health. Research in nocturnal rodents has demonstrated that when alcohol is consumed, it reaches the central hypothalamic circadian pacemaker (suprachiasmatic nuclei) and can directly alter circadian phase shifts to light. In two separate studies, we examined, for the first time, the effects of a single dose of alcohol on circadian phase advances and phase delays to light in humans. Two 23-day within-subjects placebo-controlled counterbalanced design studies were conducted. Both studies consisted of 6 days of fixed baseline sleep to stabilize circadian timing, a 2-day laboratory session, a 6-day break, and a repeat of 6 days of fixed sleep and a 2-day laboratory session. In the phase advance study ( n = 10 light drinkers, 24–45 yr), the laboratory sessions consisted of a baseline dim light phase assessment, sleep episode, alcohol (0.6 g/kg) or placebo, 2-h morning bright light pulse, and final phase assessment. In the phase-delay study ( n = 14 light drinkers, 22–44 yr), the laboratory sessions consisted of a baseline phase assessment, alcohol (0.8 g/kg) or placebo, 2-h late night bright light pulse, sleep episode, and final phase assessment. In both studies, alcohol either increased or decreased the observed phase shifts to light (interaction P ≥ 0.46), but the effect of alcohol vs. placebo on phase shifts to light was always on average smaller than 30 min. Thus, no meaningful effects of a single dose of alcohol vs. placebo on circadian phase shifts to light in humans were observed.


1977 ◽  
Vol 70 (1) ◽  
pp. 183-194
Author(s):  
JACK A. BENSON ◽  
JON W. JACKLET

1. The circadian rhythm of CAP frequency recorded from the optic nerve of isolated eyes at 15 °C was damped out by constant illumination (1100 lux) after several cycles of the rhythm. During illumination (LL) the rhythm was skewed with a rapid rising phase and slow falling phase, and the period was decreased by about 1 h. It is postulated that the circadian clock was stopped by LL at its lowest phase point, and that following cessation of LL, the rhythm was reinitiated from this phase point after a latency of 6-8 h. 2. For light pulses of 80 lux and 1100 lux, the photoresponse of the dark-adapted eye to 20 min light pulses applied beginning at 2 h intervals was not influenced by the circadian clock. At 5 lux there was a periodicity in the magnitude of the photoresponse, in phase with the circadian rhythm of spontaneous CAP production. 3. Small CAPs of non-circadian frequency were recorded together with normal CAPs in about 10% of records of output from isolated eyes. The cells producing the small CAPs had a different temperature sensitivity from those producing normal CAPs. The response of these cells to short light pulses consisted of a phasic burst of activity at light onset, followed by silence during the remainder of the short light pulse, and for 1 or 2 min following cessation of illumination. These small CAPs may be the activity either of H-type receptors or of secondary cells desynchronized from the major population. Note: Laboratory of Sensory Sciences, University of Hawaii at Manoa, 1993 East-West Road, Honolulu, Hawaii 96822, U.S.A.


1996 ◽  
Vol 271 (3) ◽  
pp. R579-R585 ◽  
Author(s):  
S. Honma ◽  
Y. Katsuno ◽  
K. Shinohara ◽  
H. Abe ◽  
K. Honma

Extracellular concentrations of glutamate and aspartate were measured in the vicinity of rat suprachiasmatic nucleus (SCN) by means of in vivo microdialysis. The concentrations of both excitatory amino acids (EAAs) were higher during the dark phase than during the light under the light-dark cycle, showing pulsatile fluctuations throughout the day. When rats were released into the complete darkness, the 24-h pattern in the aspartate continued for at least one cycle, whereas that in the glutamate disappeared. The nocturnal increases in the EAA levels were not due to the increase of locomotor activity during the nighttime, because the 24-h rhythms were also detected in animals under urethan anesthesia. The patterns of extracellular EAA levels were changed when rats were released into the continuous light. Circadian rhythm was not detected in the glutamate, whereas the 24-h pattern was maintained in the aspartate with the levels increased to various extents. A 30-min light pulse given either at zeitgber time (ZT) 1 or ZT 13 elevated the EAA levels during the latter half of the light pulse, except glutamate by a pulse at ZT 1. The extracellular EAA levels in the vicinity of the rat SCN showed the circadian rhythm with a nocturnal peak and increased in response to the continuous light and a brief light pulse. The aspartate level is considered to be regulated by the endogenous circadian rhythm, but the glutamate levels seems to be modified by the light-dark cycle.


PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0122570 ◽  
Author(s):  
Laura Herrero ◽  
Lorea Valcarcel ◽  
Crhistiane Andressa da Silva ◽  
Nerea Albert ◽  
Antoni Diez-Noguera ◽  
...  

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