Impaired daily glucocorticoid rhythm in Per1 Brd mice

Dallmann, Robert; Touma, Chadi; Palme, Rupert; Albrecht, Urs; Steinlechner, Stephan

doi:10.1007/s00359-006-0114-9

Cited by 94 publications

(76 citation statements)

References 39 publications

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“…This observation disagrees with the finding by Dallmann et al (2006), where Brdm1 mutants and wild type (wt) littermate mice. Data depict mean + SEM of reinforced lever presses for each group.…”

Section: Discussioncontrasting

confidence: 98%

Ethanol self-administration and reinstatement of ethanol-seeking behavior in Per1 Brdm1 mutant mice

et al. 2006

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Rationale Alcohol consumption shows circadian rhythmicity, i.e., alcohol preference and intake change with circadian time. Circadian rhythmicity is controlled by a biological clock, which has been shown to govern behavioral, physiological, and hormonal processes in synchronization with internal as well as external cues. Molecular components of the clock include circadian clock genes such as period (Per) 1, 2, and 3. Previously, our lab demonstrated the involvement of mouse Per1 (mPer1) and Per2 (mPer2) in modulating cocaine sensitization and reward. What is more, we investigated voluntary alcohol consumption in Per2Brdm1 mice with the results suggesting a relationship between this circadian clock gene and ethanol consumption. Objective To further complement the mPer2 study, our lab proceeded to assess mPer1's possible role on alcohol intake using operant and free choice two bottle paradigms. Methods Using operant conditions, Per1Brdm1 and wild type mice were trained to self-administer ethanol (10%) under a fixed ratio 1 (FR1) paradigm. This was ensued by a progressive ratio (PR) schedule. Furthermore, extinction sessions were introduced, followed by reinstatement measures of ethanol-seeking behavior. In another set of animals, the mice were exposed to voluntary long-term alcohol consumption, ensued by a 2-month deprivation phase, after which the alcohol deprivation effect (ADE) was measured. Results Mutant mice did not display a significantly divergent number of reinforced lever presses (FR1 and PR) than wild type animals. Furthermore, no significant differences between groups were obtained regarding reinstatement of ethanol-seeking behavior. Similar results were obtained in the two bottle free choice paradigm. Specifically, no genotype differences concerning consumption and preference were observed over a broad range of different ethanol concentrations. Moreover, after the deprivation phase, both groups exhibited significant ADEs, yet no genotype differences. Conclusions Contrary to the mPer2 data, the present findings do not suggest a relationship between the circadian clock gene mPer1 and ethanol reinforcement, seeking, and relapse behavior.

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Section: Discussioncontrasting

confidence: 98%

Ethanol self-administration and reinstatement of ethanol-seeking behavior in Per1 Brdm1 mutant mice

et al. 2006

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“…Deletion of clock genes causes pronounced cognitive and behavioural effects throughout the animal kingdom [41]. Period1-deficient mice display alterations in glucocorticoid rhythmicity [42], addiction [43], muscle strength [44], colonic motility [45], fertility [17,46] and memory [16].…”

Section: (B) Innate Routine Behaviour In Laboratory Micementioning

confidence: 99%

The clock genePeriod1regulates innate routine behaviour in mice

et al. 2014

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Laboratory mice are well capable of performing innate routine behaviour programmes necessary for courtship, nest-building and exploratory activities although housed for decades in animal facilities. We found that in mice inactivation of the clock gene Period1 profoundly changes innate routine behaviour programmes like those necessary for courtship, nest building, exploration and learning. These results in wild-type and Period1 mutant mice, together with earlier findings on courtship behaviour in wild-type and period-mutant Drosophila melanogaster, suggest a conserved role of Period-genes on innate routine behaviour. Additionally, both per-mutant flies and Period1-mutant mice display spatial learning and memory deficits. The profound influence of Period1 on routine behaviour programmes in mice, including female partner choice, may be independent of its function as a circadian clock gene, since Period1-deficient mice display normal circadian behaviour.

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“…Disruption of Per2 expression results in reduced fasting glycemia, altered glycogen accumulation in the liver, enhanced glucose-induced insulin secretion and impaired gluconeogenesis (Schmutz et al, 2010;Zani et al, 2013;Zhao et al, 2012), although Feillet et al (2006) detected no change in the daily variations of liver glycogen in Per2 mutant mice. Mice deficient in Per2 also may have dampened corticosterone rhythms ), but other investigations reported unaltered or increased corticosterone rhythms in Per2 mutants (Dallmann et al, 2006). Glucose metabolism is also severely affected in Cry mutant mice.…”

Section: Role Of Clock Components In Glucose Metabolismmentioning

confidence: 96%

Circadian rhythms in glucose and lipid metabolism in nocturnal and diurnal mammals

Jha

Challet

Kalsbeek

2015

Molecular and Cellular Endocrinology

189

129

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a b s t r a c tMost aspects of energy metabolism display clear variations during day and night. This daily rhythmicity of metabolic functions, including hormone release, is governed by a circadian system that consists of the master clock in the suprachiasmatic nuclei of the hypothalamus (SCN) and many secondary clocks in the brain and peripheral organs. The SCN control peripheral timing via the autonomic and neuroendocrine system, as well as via behavioral outputs. The sleepewake cycle, the feeding/fasting rhythm and most hormonal rhythms, including that of leptin, ghrelin and glucocorticoids, usually show an opposite phase (relative to the lightedark cycle) in diurnal and nocturnal species. By contrast, the SCN clock is most active at the same astronomical times in these two categories of mammals. Moreover, in both species, pineal melatonin is secreted only at night. In this review we describe the current knowledge on the regulation of glucose and lipid metabolism by central and peripheral clock mechanisms. Most experimental knowledge comes from studies in nocturnal laboratory rodents. Nevertheless, we will also mention some relevant findings in diurnal mammals, including humans. It will become clear that as a consequence of the tight connections between the circadian clock system and energy metabolism, circadian clock impairments (e.g., mutations or knock-out of clock genes) and circadian clock misalignments (such as during shift work and chronic jet-lag) have an adverse effect on energy metabolism, that may trigger or enhancing obese and diabetic symptoms.

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Impaired daily glucocorticoid rhythm in Per1 Brd mice

Cited by 94 publications

References 39 publications

Ethanol self-administration and reinstatement of ethanol-seeking behavior in Per1 Brdm1 mutant mice

Ethanol self-administration and reinstatement of ethanol-seeking behavior in Per1 Brdm1 mutant mice

The clock genePeriod1regulates innate routine behaviour in mice

Circadian rhythms in glucose and lipid metabolism in nocturnal and diurnal mammals

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