Pineal melatonin synthesis is altered in Period1 deficient mice

Christ, Elmar; Pfeffer, Martina; Korf, Horst‐Werner; Gall, Charlotte von

doi:10.1016/j.neuroscience.2010.09.009

Cited by 36 publications

(24 citation statements)

References 44 publications

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“…Thus the robust daily rhythm of Per1 and Aa-nat expression in the pineal gland in vivo is most likely driven by the adrenergic input from SCN. Therefore, although a recent study in Per1- deficient mice suggested a role for PER1 in the modulation of the rhythmic melatonin synthesis in the pineal gland [28], the function of the pineal clockwork is presently unknown.…”

Section: Discussionmentioning

confidence: 99%

A Noradrenergic Sensitive Endogenous Clock Is Present in the Rat Pineal Gland

et al. 2011

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The aim of this study was to examine the occurrence of endogenous oscillations of Per1, Per2, Bmal1 and Rev-erbα genes in rat pineal explants and to investigate their regulation by adrenergic ligands. Our results show a significant and sustained rhythm of Per2,Bmal1 and Rev-erbα gene expression for up to 48 h in cultured pineal gland with a pattern similar to that observed in vivo. By contrast, the rhythms of Per1 and Aa-nat, the rate-limiting enzyme for melatonin synthesis, were strongly attenuated after 24 h in culture. Addition of the exogenous adrenergic agonist isoproterenol on cultured pineal glands induced a short-term increase in mRNA levels of Per1 and Aa-nat, but not those of Per2,Bmal1 and Rev-erbα. This study demonstrates that the rat pineal gland hosts a circadian oscillator as evidenced by the sustained, noradrenergic-independent, endogenous oscillations of Per2, Bmal1 and Rev-erbα mRNA levels in cultured tissues. Only expression of Per1 was stimulated by adrenergic ligands suggesting that, in vivo, the adrenergic input could synchronize the pineal clock by acting selectively on Per1.

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Section: Discussionmentioning

confidence: 99%

A Noradrenergic Sensitive Endogenous Clock Is Present in the Rat Pineal Gland

et al. 2011

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“…This melatonin synthesis delay in Syrian hamsters is attributed to noradrenaline inducing the clock gene Per1 at the beginning of darkness (Wongchitrat et al 2009), which blocks the transcription of key enzymes in melatonin synthesis (Christ et al 2010). NFKB has been reported to inhibit the melatonin biosynthetic pathway in cultured rat pineal glands .…”

Section: Discussionmentioning

confidence: 99%

Plasma corticosterone elevation inhibits the activation of nuclear factor kappa B (NFKB) in the Syrian hamster pineal gland

Ferreira¹,

Bothorel

Markus

et al. 2011

Stress

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We evaluated how the mild stress-induced increase in endogenous corticosterone affected the pineal gland in Syrian hamsters (Mesocricetus auratus). The animals were maintained under constant light for 1 day, instead of a cycle of 14:10-h, to increase the circulating corticosterone levels during the daytime. The nuclear translocation of nuclear factor kappa B (NFKB), which is the pivotal transcription factor for stress and injury, presented a daily rhythm in normal animals. NFKB nuclear content increased linearly from the onset of light [Zeitgeber Time 0 (ZT0)] until ZT11 and decreased after ZT12 when the plasma corticosterone peak was detected in normal animals. However, the 24-h profiles of the two curves were different, and they did not clearly support an exclusive relationship between corticosterone levels and NFKB content. Therefore, we tested the effect of increased endogenous corticosterone through inducing mild stress by maintaining daytime illumination for one night. This stressful condition, which increased daytime corticosterone levels, resulted in a daytime decrease in NFKB nuclear content, and this was inhibited by mifepristone. Overall, this study shows that NFKB has a daily rhythm in Syrian hamster pineal glands and, by increasing endogenous corticosterone with a stressful condition, NFKB activity is regulated. Therefore, this study suggests that the pineal gland in the Syrian hamster is a sensor of stressful conditions.

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“…More recently, it has been demonstrated that the melatonin biosynthesis pathway can genetically suppress the circadian perturbations of Clock-D19 mutation (Shimomura et al 2010), suggesting a role of melatonin in contributing to the robustness of the SCN clock (see below). PER1 deficiency has been shown to enhance Aanat transcription, enzymatic activity and hence melatonin secretion (Chen & Baler 2000, Christ et al 2010. In CRY1/2 double-deficient mice on a melatonin-proficient genetic background not only is the melatonin rhythm blunted under light-dark conditions, but also photic suppression of melatonin is abolished (Yamanaka et al 2010).…”

Section: Scn-pineal Interactionmentioning

confidence: 99%

Interactions between endocrine and circadian systems

Tsang¹,

Barclay

Oster

2013

Journal of Molecular Endocrinology

101

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In most species, endogenous circadian clocks regulate 24-h rhythms of behavior and physiology. Clock disruption has been associated with decreased cognitive performance and increased propensity to develop obesity, diabetes, and cancer. Many hormonal factors show robust diurnal secretion rhythms, some of which are involved in mediating clock output from the brain to peripheral tissues. In this review, we describe the mechanisms of clock-hormone interaction in mammals, the contribution of different tissue oscillators to hormonal regulation, and how changes in circadian timing impinge on endocrine signalling and downstream processes. We further summarize recent findings suggesting that hormonal signals may feed back on circadian regulation and how this crosstalk interferes with physiological and metabolic homeostasis.

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Pineal melatonin synthesis is altered in Period1 deficient mice

Cited by 36 publications

References 44 publications

A Noradrenergic Sensitive Endogenous Clock Is Present in the Rat Pineal Gland

A Noradrenergic Sensitive Endogenous Clock Is Present in the Rat Pineal Gland

Plasma corticosterone elevation inhibits the activation of nuclear factor kappa B (NFKB) in the Syrian hamster pineal gland

Interactions between endocrine and circadian systems

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