Maturation of Adrenal Stress Responsiveness in the Rat

Schoenfeld, Nancy M.; Leathem, James H.; Rabii, Jamshid

doi:10.1159/000123058

Cited by 97 publications

(57 citation statements)

References 16 publications

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“…Manin and DeLost (24) demonstrated that neurotrophic stress increased MCR through increased Vd in the conscious guinea pig. Given the developmental increase in the stress response in the rat (1,25), similar effects on MCR and Vd would result in a pattern of response opposite to that seen in Figure I. Finally, Herbst et al (26) showed that repeated anesthesia in adult rats had no effect on in vitro reduction of ring A of corticosterone.…”

Section: Discussionmentioning

confidence: 93%

Kinetics of Circulating Corticosterone in Infant Rats

1988

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ABSTRACT. Corticosterone plays an important role in the regulation of postnatal development in the rat. Basal concentrations of plasma corticosterone increase markedly during the 3rd wk of life. To date, however, the physiologic bases of this increase have remained unclear. To understand the determinants of circulating concentrations of corticosterone during this period, the plasma half-life of disappearance at steady state (tlh), the apparent volume of distribution, and metabolic clearance rate were determined after injection of a tracer dose of 3H-corticosterone in rats at 12, 16, and 22 days of age. The tlh for total plasma corticosterone decreased with increasing age. The volume of distribution decreased even more steeply and, consequently, the MCR displayed a highly significant decline between 12 and 22 days of age. As plasma concentrations of corticosteroid-binding globulin are known to increase markedly during this period, the t~ of protein-bound corticosterone was measured and that of free corticosterone was computed. At all ages the tth of bound corticosterone was less than that of free corticosterone. Protein binding of the injected 3H-corticosterone increased significantly with development. Thus, increased binding of corticosterone is associated with decreased t~. The increasing association of corticosterone with corticosteroid-binding globulin during this developmental period is the most likely explanation for the steep decline of volume of distribution and thus of the metabolic clearance rate for corticosterone. The latter provides, for the first time, an understanding of the basis of the developmental increase in plasma concentrations of corticosterone. (Pediatr Res 24: 595-599,1988)

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Section: Discussionmentioning

confidence: 93%

Kinetics of Circulating Corticosterone in Infant Rats

1988

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“…Furthermore, peak levels of BrdU-labeled cells in the dentate gyrus occur between P9-11 (Liu et al 2003) and P11 is the day at the beginning of the critical period for MA-induced long-term cognitive deficits (Vorhees et al 1994Williams et al 2002Williams et al , 2003bWilliams et al ,c, 2004b. Similar to the effects of MA, other factors such as corticotropin-releasing factor (Walker et al 1986) or various stressors (Schoenfeld et al 1980) administered during the neonatal period can be described as producing a U-shaped curve response pattern of corticosterone release. In the current study we also demonstrated this Ushaped corticosterone response to MA treatment.…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of the adrenal response to (+)-methamphetamine in neonatal rats: The effect of prior drug exposure

Williams

Schaefer

Furay

et al. 2006

Stress

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We examined the ontogeny of the corticosterone response to (+)-methamphetamine in neonatal rats. In experiment-1, animals were injected with 10 mg/kg of (+)-methamphetamine or saline and plasma corticosterone levels were examined in separate groups 30 or 105 min later on postnatal day (P) 1, 3, 5, 7, 9, 11, 13, 15, 17, or 19. The adrenal response to methamphetamine was best described by a U-shaped function with the nadir of corticosterone release occurring between P7 and P13. Experiment-2 was similar except that the effect of four consecutive days of exposure to (+)-methamphetamine (four times daily at 2 h intervals with 10 mg/kg) was assessed with a single final dose early on the fifth day (i.e. P1-5, 3-7, 5-9, 7-11, 9-13, 11-15, 13-17, 15-19). The 30 min corticosterone response after multiple methamphetamine doses was augmented compared to single exposures, with the exception of the two earliest dosing intervals ending on P5 and P7, where the responses were lower. In addition, at 105 min, the levels of corticosterone were attenuated relative to a single drug administration. With the exception of animals receiving methamphetamine from P15 to P19, thymus weights were unaffected. The data demonstrate that (+)-methamphetamine is a robust activator of corticosterone release in developing animals and this release is extensively modified by age and previous drug exposure.

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“…During this period, basal circulating corticosterone levels are very low and mild stressors are unable to induce a peripheral corticosterone response (Levine et al 2000). However, a variety of severe or prolonged stressors disrupt the quiescence of the hypothalamic-pituitary-adrenal (HPA) axis during this time of development (Schoenfeld et al 1980, Walker et al 1991, Yi & Baram 1994. The high levels of circulating corticosterone induced by these treatments are usually seen as the cause for a consequently altered developmental trajectory and finally persistent consequences in the adult animal.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y mediates the initial hypothalamic–pituitary–adrenal response to maternal separation in the neonatal mouse

Schmidt¹,

Liebl²,

Sterlemann³

et al. 2008

Journal of Endocrinology

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The function of the hypothalamic-pituitary-adrenal (HPA) axis of the neonatal mouse or rat is characterized by a period of quiescence, where mild stimuli are unable to elicit a pronounced increase in circulating corticosterone. A disruption of this period by maternal separation has been shown to result in a variety of long-term consequences, including neuroendocrine and behavioral disturbances. We have recently shown that peripheral metabolic markers like glucose or ghrelin are altered by maternal separation and that these changes precede the effects on corticosterone secretion. In the current study, we investigated whether the initial activation of the HPA axis is mediated via neuropeptide Y (NPY). To test this hypothesis, we studied the effects of an 8 h maternal separation in NPY-deficient mice. In addition, we compared the effect of the genotype with the previously described pharmacological effect of a ghrelin receptor antagonist. We could show that the peripheral response to maternal separation is decreased in NPY heterozygous and homozygous animals. In addition, maternal separation effects on corticotropin releasing hormone and glucocorticoid receptor expression in the brain were prevented in NPYdeficient pups. These effects were similar to a pharmacological ghrelin receptor blockade. We conclude that metabolic signals via an NPY-mediated pathway play a crucial role in activating the stress system of the neonatal mouse.

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Maturation of Adrenal Stress Responsiveness in the Rat

Cited by 97 publications

References 16 publications

Kinetics of Circulating Corticosterone in Infant Rats

Kinetics of Circulating Corticosterone in Infant Rats

Ontogeny of the adrenal response to (+)-methamphetamine in neonatal rats: The effect of prior drug exposure

Neuropeptide Y mediates the initial hypothalamic–pituitary–adrenal response to maternal separation in the neonatal mouse

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