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Interplay between adenosine signaling and the circadian system
Škrle, Jan ; Bendová, Zdeňka (advisor) ; Houdek, Pavel (referee)
Sleep is regulated primarily by the two processes, by Process C and S. Process C represents circadian regulation by circadian system; Process S represents the homeostatic sleep drive. Circadian system controls the timing of many physiological functions including body temperature rhythms, locomotor activity rhythms, periodically changing hormones levels etc. Process C contributes to sleep regulation mainly by setting lower and upper thresholds for a sleep pressure. When the sleep pressure reaches one of these thresholds, falling asleep or waking is promoted. However, the sleep architecture is altered by a phase of endogenous oscillators as well. The homeostatic sleep drive is based on a sleep- wake history with the sleep pressure rising during a wakefulness and lowering during sleep. This mechanism is responsible for a modification in structure of a recovery sleep following a sleep deprivation. Due to the effects of adenosine on sleep regulation, adenosine signalling is considered to play a critical role in the homeostatic sleep drive. These two processes were thought to be independent of each other, but new data show that there is a reciprocal regulation between them. The aim of this work was to conclude, where these two processes meet, with a special attention on processes, where the adenosine...
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Effect of ketamine on light-induced changes in the circadian system
Kratina, Alex ; Bendová, Zdeňka (advisor) ; Valeš, Karel (referee)
The circadian system is controlled by the suprachiasmatic nuclei of the hypothalamus (SCN) and ensures optimal timing of physiological processes. Synchronization of this system with external light conditions is based on the activation of NMDA receptors during light exposure in the subjective night. Ketamine is a non-competitive antagonist of NMDA receptors used as a safe anesthetic, whose subanesthetic doses act as an antidepressant with a rapid onset of action, and increase proliferation in some parts of the brain. There are hypotheses about the possible effect of subanesthetic doses of ketamine on the circadian system, altough this effect has not yet been tested. This work aims to investigate the effect of a single subanesthetic dose of ketamine on the circadian system of the rat, especially on light-induced changes in locomotor activity and light-induced markers in the SCN and dentate gyrus, which represents one of the strongly proliferative areas of the brain. Our results show that ketamine decreases light pulse-induced c-FOS protein expression in the SCN at the onset of the subjective night, but increases this expression in the dentate gyrus under the same conditions. Reduction of c-FOS expression in the SCN correlates with the behavioral output of the circadian system and thus suppresses the...
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The effect of endocannabinoid system on light entrainment of rat circadian system
Filipovská, Eva ; Bendová, Zdeňka (advisor) ; Balík, Aleš (referee)
Circadian system of mammals is generated in suprachiasmatic nuclei of hypothalamus. This system is synchronized with light conditions through phase shifts that occur after light exposition during the subjective night. Recent studies have shown that activation of endocannabinoid receptors attenuates the light-induced phase shifts and influences the ability of circadian system to light entrainment. The aim of this work is to examine this influence on behavioral level and on light-reactive cellular processes within the suprachiasmatic nuclei. Our results show that the activation of endocannabinoid system via CB1 receptor agonist modulates the light-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and the expression of c-Fos protein in neurons of suprachiasmatic nuclei in the rat's brain; these cellular processes correlate with the attenuation of light entrainment. Keywords: circadian system, suprachiasmatic nuclei, light entrainment, endocannabinoid system, CB1 receptors, extracellular signal-regulated kinase 1/2, ERK1/2, c-Fos
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