Circadian pacemaker

Dijk, D. J. Czeisler, C. A. (1995). Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephahc slow waves, and sleep spindle activity in humans. J. Neurosci. 15, 3526-38. 

Strogatz S. H., Kronauer R. E., Czeisler C. A. (1987). Circadian pacemaker interferes with sleep onset at specific times each day role in insomnia. Am. J. Physiol 253(1), R172-8. 

The sleepiness associated with narcolepsy may result from impaired circadian influences (Broughton et al, 1998), particularly of the circadian alertness signal which contributes to the timing and consolidation of the sleep period (Dijk Czeisler, 1994 Edgar et al, 1993). Confirmatory data for this hypothesis was provided by Dantz et al. (1994), who, using a forced desynchrony protocol, showed that narcoleptic patients have a normal circadian pacemaker and homeostatic sleep drive, but a deficit in alertness associated with the circadian signal. Although results are more difficult to interpret in an animal with... 

Lesions of serotonergic neurons in laboratory animals have been reported by some, but not all, investigators to disrupt locomotor rhythms or to result in the loss of the daily rhythm of corticosterone. There is evidence that, in the hamster, the median raphe nucleus projects to the SCN whereas the dorsal raphe nucleus innervates the IGL furthermore, the serotonergic innervation to the SCN and not the IGL is necessary for the photic entrainment of locomotor activity [22]. It appears then, that the SCN circadian pacemaker or clock is modulated by stimulation of serotonergic receptors in the SCN and that serotonergic projections to the SCN may modulate the phase of the SCN in intact animals. 

R. E. Kronauer, D. B. Forger, and M. E. Jewett, Quantifying human circadian pacemaker response to brief, extended, and repeated light stimuli over the phototopic range. J. Biol. Rhythms 14, 500-515 (1999). 

Circadian clock-controlled rhythms provide most organisms with an orchestrated temporal programme that allows for appropriate timing of physiology (i.e. blood pressure, hormonal levels) and behaviour (i.e. alertness, sleep-wake cycle). The mammalian central circadian pacemaker resides in the suprachiasmatic nucleus (SCN) of the brain (Weaver 1998). At the molecular level, the core oscillator driving the mammahan clock consists of interconnected autoregulatory... 

Bunger MK, Wilsbacher LD, Moran SM et al 2000 Mop3 is an essential component of the master circadian pacemaker in mammals. Cell 103 1009—1017 Cermakian N, Sassone-Corsi P 2002 Environmental stimulus perception and control of circadian clocks. Curr Opin Neurobiol 12 359—365... 

Dunlap JC 2003 Molecular biology of circadian pacemaker systems. In Dunlap JC, Loros JJ, Decoursey P (eds) Chronobiology biological timing. Sinauer Assoc, Sunderland MA,... 

Schibler U, Sassone-Corsi P 2002 A web of circadian pacemakers. Cell 111 919—922 Stirland JA, Hastings MH, Loudon AS, Maywood ES 1996 The tau (r) mutation in the Syrian hamster alters the photoperiodic responsiveness of the gonadal axis to melatonin signal frequency. Endocrinology 137 2183-2186... 

Glossop NR, Lyons LC, Hardin PE 1999 Interlocked feedback loops within the Drosophila circadian pacemaker. Science 286 766—768... 

Pittendrigh CS, Daan S 1976a A functional analysis of circadian pacemakers in nocturnal rodents. 1. The stability and lability of spontaneous frequency. J Comp Physiol A 106 223-252 Pittendrigh CS, Daan S 1976b A functional analysis of circadian pacemakers in nocturnal rodents. IV. Entrainment pacemaker as clock. J Comp Physiol [A] 106 291—331 Ralph MR, Foster RG, Davis FC, Menaker M 1990 Transplanted suprachiasmatic nucleus determines circadian period. Science 247 975-978 Redlin U, Mrosovsky N 1999 Masking by light in hamsters with SCN lesions. J Comp Physiol [A] 184 439-448... 

Lewy AJ, Sack RL, Blood ML, et al. Melatonin marks circadian phase position and resets the endogenous circadian pacemaker in humans. Ciba Found Symp 1995 183 303-321. 

Interaction of homeostatic sleep drive and endogenous circadian pacemaker Total sleep deprivation... 

As noted earlier, an effective assay of the cognitive impact of sleep loss should be sensitive to the homeostatic drive for sleep in interaction with the endogenous circadian pacemaker (33,58). From Figure 3, it is evident that the PVT fulfills this requirement, with performance during 88 hr of sleep deprivation demonstrating both a monotonic component to impairment, which increases with increasing time awake, and a rhythmic oscillation in performance, which fluctuates in daily cycles. 

Daan S, Beersma DG, Borbely A A. Timing of human sleep recovery process gated by a circadian pacemaker, Am J Physiol 1984 246 R161-83. 

Czeisler CA, Duffy JF, Shanahan TL, Brown EN, Mitchell JF, Rimmer DW, Rhonda JM, Silva EJ, Allan JS, Emens JS, Dijk DJ, Kronauer RE. Stability, precision, and near-24-hour period of the human circadian pacemaker. Science 1999 284 2177-2181. 

Jovanovska A, Prosser RA. Translational and transcriptional inhibitors block serotonergic phase advances of the suprachiasmatic nucleus circadian pacemaker in vitro. J Biol Rhythms 2002 17 137-146. 

The autonomous functions exhibit circadian rhythms which are under the control of a neuronal pacemaker, located in the suprachiasmatic nuclei (SCN) of the hypothalamus. The circadian pacemaker arises from complex dynamics of gene expression and is synchronized to the external light. In the case of mental disorders, the regular rhythms of autonomous functions are obviously disturbed which led to the formulation of the desynchronization hypotheses [8, 9], This does not necessarily contradict the transmitter hypothesis . Transmitter imbalance, of course, also interferes with the inherent system dynamics and can change the endogenous rhythmicity, eventually with the result of desynchronization. A first computational approach which simulates the rhythmicity of the HPA axis and its alterations with scaling of transmitter mediated positive and negative feedback loops is briefly summarized in the second Results section. 

The hypothalamus releases CRH depending on the circadian pacemaker C under feedback control (Fh ) from cortisol ... 

The complete system responses are determined by the interactions, i.e. resonances, between the subthreshold and event-generating mechanisms. Again, in the HPA axis model, these interactions, so far, are rather simple and unidirectional. The circadian pacemaker modulates the H PA feedback loops in a nonlinear multiplicative way but is itself not influenced by the dynamics of the cortisol releasing processes. In contrast, in the neuronal and psychiatric models, the two subsystems are interlinked by a common control variable, the membrane voltage and the disease variable, respectively. These interlinks are a major source of very complex, inclusively chaotic dynamics [96, 111, 112]. 

S. Homberg, U. Dircksen, H. Rao, K.R., in press). These investigators also found that the position and branching pattern of the PDH-IR cell group located between the lobula and medulla are the same as those proposed for circadian pacemaker neurons in crickets and cockroaches (60). 

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