Effects of Destruction of the Suprachiasmatic Nuclei on the Circadian Rhythms in Plasma Corticosterone, Body Temperature, Feeding and Plasma Thyrotropin

K, Abe; Kroning, J.; Greer, Monte A.; Critchlow, V.

doi:10.1159/000122913

Cited by 173 publications

(70 citation statements)

References 16 publications

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“…The SCN is thought to drive this rhythm, which is abolished by SCN lesions (Moore and Eichler, 1972;Abe et al, 1979;Filipski et al, 2004), through neural connections to the corticotrophin-releasing factor and arginine-vasopressin neurons of the paraventricular nuclei of the hypothalamus (Buijs et al, 1993) and probably also through the sympathetic innervation of the adrenal gland (Jasper and Engeland, 1994). Although the activity of the SCN is the predominant pathway influencing the hypothalamo-pituitary-adrenal (HPA) axis under conditions of ad libitum feeding, which occurs mainly at night, restricted daytime feeding establishes a bimodal temporal pattern of corticosterone secretion in rodents (Krieger, 1974;Honma et al, 1984;Holmes et al, 1997;Balsalobre et al, 2000;Le Minh et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice

Sheward¹,

Maywood²,

French³

et al. 2007

J. Neurosci.

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The master clock driving mammalian circadian rhythms is located in the suprachiasmatic nuclei (SCN) of the hypothalamus and entrained by daily light/dark cycles. SCN lesions abolish circadian rhythms of behavior and result in a loss of synchronized circadian rhythms of clock gene expression in peripheral organs (e.g., the liver) and of hormone secretion (e.g., corticosterone). We examined rhythms of behavior, hepatic clock gene expression, and corticosterone secretion in VPAC 2 receptor-null (Vipr2 Ϫ/Ϫ ) mice, which lack a functional SCN clock. Unexpectedly, although Vipr2 Ϫ/Ϫ mice lacked robust circadian rhythms of wheel-running activity and corticosterone secretion, hepatic clock gene expression was strongly rhythmic, but advanced in phase compared with that in wild-type mice. The timing of food availability is thought to be an important entrainment signal for circadian clocks outside the SCN. Vipr2 Ϫ/Ϫ mice consumed food significantly earlier in the 24 h cycle than wild-type mice, consistent with the observed timing of peripheral rhythms of circadian gene expression. When restricted to feeding only during the daytime (RF), mice develop rhythms of activity and of corticosterone secretion in anticipation of feeding time, thought to be driven by a food-entrainable circadian oscillator, located outside the SCN. Under RF, mice of both genotypes developed food-anticipatory rhythms of activity and corticosterone secretion, and hepatic gene expression rhythms also became synchronized to the RF stimulus. Thus, food intake is an effective zeitgeber capable of coordinating circadian rhythms of behavior, peripheral clock gene expression, and hormone secretion, even in the absence of a functional SCN clock.

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Section: Discussionmentioning

confidence: 99%

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice

Sheward¹,

Maywood²,

French³

et al. 2007

J. Neurosci.

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“…More specifically, the diurnal rhythm of corticosteroid secretion (CS), which depends on the hypothalamic-pituitary-adrenal axis, stems from the SCN. After destruction of these nuclei the corticosterone levels lose the circadian rhythm and remain in the morning range concentrations (Moore and Eichler, 1972;Coen and MacKinnon, 1976;Abe et al, 1979) or show abnormal values (Raisman and BrownGrant, 1977;Szafarczyk et al, 1979;Kalsbeek et al, 1992). This axis can be modulated by regulating either the corticotrophin-releasing hormone (CRH) produced by the paraventricular nucleus (PVN) of the hypothalamus or the adrenocorticotrophic hormone (ACTH) in the pituitary gland.…”

Section: Introductionmentioning

confidence: 99%

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release

et al. 1997

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Arginine vasopressin (AVP) produced in the hypothalamic suprachiasmatic nuclei (SCN) plays a role in establishing neuroendocrine rhythms and, in particular, in regulating the corticotrope axis rhythm. It has recently been shown that AVP from SCN inhibits corticosteroid release. In order to investigate the influence of suprachiasmatic AVP on the different peptidergic systems through the hypothalamus, SCN neurons containing AVP were functionally lesioned by using toxins associated with a cytotoxic monoclonal antibody (MAb) raised against AVP. Six days later, the AVP contents and AVP mRNA were measured in different hypothalamic and extrahypothalamic sites. Adrenocorticotrophic hormone (ACTH) concentration was also measured in plasma. Microinjection of the AVP-MAb/toxin mixture into SCN brought about a significant decrease in the AVP expression in SCN. This is demonstrated by the decrease in the AVP immunoreactive content (24%, P < 0.01) and the decrease of AVP hybridized mRNA (33%, P < 0.01). This points to the efficiency of the microinjection in decreasing the production of AVP in the injection area. Modifications of the AVP contents in the two subdivisions of the hypothalamic paraventricular nucleus (PVN) were also observed. AVP contents decreased in the parvocellular subdivision (pPVN); this is coherent with the AVP depletion in SCN since pPVN is the major site of the SCN hypothalamic efferences. AVP content and AVP mRNA increased in the magnocellular subdivision (mPVN); this also confirms the difference in AVP synthesis regulation according to the PVN subdivisions. The microinjection did not modify AVP expression in supraoptic nuclei or oxytocin (OT) immunoreactive content in the main hypothalamic OT containing sites. Plasma ACTH values were double (P < 0.02) the values measured under non-specific IgG treatment 10 hr after lights on. This probably resulted from the stimulation of the hypothalamo-pituitary-adrenal system since corticotrophin-releasing hormone (CRH) mRNA increased simultaneously by 24% (P < 0.05) in the PVN and the immunoreactive CRH content of the median eminence significantly decreased (26%, P < 0.05). Overall, our data confirm that AVP produced in the SCN inhibits the CRH-adrenocorticotrope axis in normal conditions, probably because of SCN projections of AVP neurons on the PVN.

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“…Although the function of this oscillation in secretion is not well understood, it is thought to be important for energy balance, because diet and feeding time have an impact on secretion rhythm (5)(6)(7). Diet composition (8) and timing of feeds have also been shown to modulate the circadian pacemaker (9,10), and a connection between the pacemaker and the oscillations in glucocorticoid secretion has been observed (8,11,12). In turn, glucocorticoids can themselves induce cycling of circadian clock components in peripheral tissues, suggesting that there are situations in which glucocorticoids may dictate cycling rhythmicity (13).…”

mentioning

confidence: 99%

Glucocorticoid regulation of the circadian clock modulates glucose homeostasis

Bernal²,

Pillsbury³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

347

291

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Circadian clock genes are regulated by glucocorticoids; however, whether this regulation is a direct or secondary effect and the physiological consequences of this regulation were unknown. Here, we identified glucocorticoid response elements (GREs) at multiple clock genes and showed that 3 were directly regulated by the glucocorticoid receptor. We determined that a GRE within the core clock gene Per2 was continuously occupied during rhythmic expression and essential for glucocorticoid regulation of that gene in vivo. We further demonstrated that mice with a genomic deletion spanning this GRE expressed elevated leptin levels and were protected from glucose intolerance and insulin resistance on glucocorticoid treatment but not from muscle wasting. We conclude that Per2 is an integral component of a particular glucocorticoid regulatory pathway and that glucocorticoid regulation of the peripheral clock is selectively required for some actions of glucocorticoids.circadian rhythm ͉ diabetes ͉ nuclear receptors ͉ metabolic syndrome

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Effects of Destruction of the Suprachiasmatic Nuclei on the Circadian Rhythms in Plasma Corticosterone, Body Temperature, Feeding and Plasma Thyrotropin

Cited by 173 publications

References 16 publications

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release

Glucocorticoid regulation of the circadian clock modulates glucose homeostasis

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Effects of Destruction of the Suprachiasmatic Nuclei on the Circadian Rhythms in Plasma Corticosterone, Body Temperature, Feeding and Plasma Thyrotropin

Cited by 173 publications

References 16 publications

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC2Receptor-Null Mice

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC2Receptor-Null Mice

Arginine vasopressin (AVP) depletion in neurons of the suprachiasmatic nuclei affects the AVP content of the paraventricular neurons and stimulates adrenocorticotrophic hormone release

Glucocorticoid regulation of the circadian clock modulates glucose homeostasis

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Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice

Entrainment to Feeding but Not to Light: Circadian Phenotype of VPAC₂Receptor-Null Mice