Role of the suprachiasmatic nuclei in the circadian timing system of the squirrel monkey. I. The generation of rhythmicity

1984 ◽  
Vol 300 (2) ◽  
pp. 275-284 ◽  
Author(s):  
H. Elliott Albers ◽  
Ralph Lydic ◽  
Philippa H. Gander ◽  
Martin C. Moore-Ede
2016 ◽  
Vol 8 (1) ◽  
pp. 14-22 ◽  
Author(s):  
Navin Adhikary ◽  
Santosh Lal Shrestha ◽  
Jia Zhong Sun

1985 ◽  
Vol 249 (2) ◽  
pp. R274-R280 ◽  
Author(s):  
T. M. Hoban ◽  
F. M. Sulzman

We examined light effects on the circadian timing system of the squirrel monkey. A phase-response curve to 1-h pulses of light was constructed for the drinking rhythm of six animals. The phase-response curve was the same type as that exhibited by nocturnal rodents, with phase delays occurring early in the subjective night and phase advances late in the subjective night. The range of entrainment of 10 monkeys to days with 1 h light and x h dark was determined. Five monkeys used to generate the phase-response curve were also used in the range of entrainment determination. For short light-dark cycles the range of entrainment was smaller than that expected, with no monkey entraining to a day length of less than 23.5 h.


Author(s):  
Gabriella Lundkvist ◽  
Gene D. Block

Diurnal variations in physiology and behavior are ubiquitous in higher organisms. Although some rhythms are driven directly by geophysical cycles of light or temperature, most are generated by internal timers, commonly referred to as biological clocks. In mammals, including humans, these circadian (near 24-h) properties are controlled by a central timer formed by a distinct regional network in the anterior hypothalamus close to the optic chiasm, the bilateral suprachiasmatic nuclei (SCN). Rodents, with their SCN lesioned, fail to exhibit diurnal variations in behavior. The mechanism generating rhythmicity is contained within individual neurons; however, many of the properties of the circadian timing system derive from cellular interactions within SCN. These microcircuits give rise to a functional clock capable of maintaining a circadian rhythm with a stable period and phase and driving or synchronizing circadian rhythms in other tissues.


1999 ◽  
Vol 277 (4) ◽  
pp. R1171-R1178 ◽  
Author(s):  
Sally A. Ferguson ◽  
David J. Kennaway

Mammalian circadian rhythms are controlled by the suprachiasmatic nuclei (SCN) in concert with light information. Several neurotransmitters and neural pathways modulate light effects on SCN timing. This study used a line of rat with an upregulated cholinergic system to investigate the role of acetylcholine in rhythmicity. With the use of a selective breeding program based on the thermic response to a cholinergic agonist, we developed a supersensitive (Sox) and subsensitive (Rox) rat line. The Sox rats showed an earlier onset time of melatonin rhythm under a 12:12-h light-dark photoperiod from generation 3 (3 ± 0.5 h after dark) compared with Rox rats (4.5 ± 0.1 h) and an earlier morning decline in temperature (0.9 ± 0.3 h before lights on) compared with Rox animals (0.1 ± 0.1 h). Furthermore, the Soxanimals displayed a significantly shorter free-running period of temperature rhythm than Rox rats (23.9 ± 0.04 and 24.3 ± 0.1 h, respectively, P < 0.05). The results suggest that the altered circadian timing of the Sox rats may be related to the cholinergic supersensitivity, intimating a role for acetylcholine in the circadian timing system.


Reproduction ◽  
2006 ◽  
Vol 132 (3) ◽  
pp. 379-392 ◽  
Author(s):  
Michael J Boden ◽  
David J Kennaway

There is a growing recognition that the circadian timing system, in particular recently discovered clock genes, plays a major role in a wide range of physiological systems. Microarray studies, for example, have shown that the expression of hundreds of genes changes many fold in the suprachiasmatic nucleus, liver heart and kidney. In this review, we discuss the role of circadian rhythmicity in the control of reproductive function in animals and humans. Circadian rhythms and clock genes appear to be involved in optimal reproductive performance, but there are sufficient redundancies in their function that many of the knockout mice produced do not show overt reproductive failure. Furthermore, important strain differences have emerged from the studies especially between the variousClock(CircadianLocomotorOutputCycleKaput) mutant strains. Nevertheless, there is emerging evidence that the primary clock genes,ClockandBmal1(Brain andMuscleARNT-like protein 1, also known asMop3), strongly influence reproductive competency. The extent to which the circadian timing system affects human reproductive performance is not known, in part, because many of the appropriate studies have not been done. With the role ofClockandBmal1in fertility becoming clearer, it may be time to pursue the effect of polymorphisms in these genes in relation to the various types of infertility in humans.


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