Adrenocorticotropin,β-Endorphin, and Corticosterone Secretion in Brattleboro Rats*

Conte-Devolx, B.; Giraud, Pierre; Oliver, Charles; Castanas, Elias; Boudouresque, F; Gillioz, P.; Millet, Yves

doi:10.1210/endo-110-6-2097

Cited by 53 publications

(31 citation statements)

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“…Assays. Corticosterone was assayed in plasma and urine (after ethanol or dichloromethane extraction, respectively) using a radioimmunoassay previously described (16). Adrenals were dissected free of fat, weighed to the nearest milligram, and homogenized in a solution of 0.9% NaCl.…”

Section: Methodsmentioning

confidence: 99%

Postnatal Diet-Induced Obesity in Rats Upregulates Systemic and Adipose Tissue Glucocorticoid Metabolism During Development and in Adulthood

et al. 2005

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In humans, a hyperactivity of glucocorticoid metabolism was postulated to be involved in the intrauterine programming of the metabolic syndrome in adulthood. We studied in rats the effects of overfeeding, obtained by reducing the size of the litter in the immediate postnatal period, a time crucial for neuroendocrine maturation such as late gestation in humans. Overfeeding induced early-onset obesity and accelerated the maturation of the hypothalamo-pituitary-adrenal (HPA) axis together with an upregulation of adipose tissue glucocorticoid receptor (GR) mRNA. In adulthood, neonatally overfed rats presented with moderate increases in basal and stress-induced corticosterone secretion and striking changes in visceral adipose tissue glucocorticoid signaling, that is, enhanced GR and 11␤-hydroxysteroid dehydrogenase type 1 mRNA levels. The above-mentioned alterations in the endocrine status of overfed rats were accompanied by a moderate overweight status and significant metabolic disturbances comparable to those described in the metabolic syndrome. Our data demonstrate for the first time that postnatal overfeeding accelerates the maturation of the HPA axis and leads to permanent upregulation of the HPA axis and increased adipose tissue glucocorticoid sensitivity. Thus, the experimental paradigm of postnatal overfeeding is a powerful tool to understand the pathophysiology of glucocorticoid-induced programming of metabolic axes. Diabetes 54: [197][198][199][200][201][202][203] 2005 N umerous clinical and biological findings indicate that glucocorticoids are involved in the pathophysiology of abdominal obesity and its accompanying complications. Indeed, an excess of glucocorticoids, when associated with hyperinsulinism, favors an increase of lipogenesis and a decrease of lipolysis, together with a stimulation of hepatic neoglucogenesis and an inhibition of peripheral glucose utilization (1). Alterations in the hypothalamo-pituitary-adrenal (HPA) axis have been described in human obesity and in rodent models of obesity. They could involve a hyperactivity of the central command of ACTH secretion, secondary to an increased exposure or sensitization to stress (2) or decreased negative glucocorticoid feedback (3). In addition, changes in peripheral glucocorticoid signaling with increased visceral adipose tissue glucocorticoid receptor (GR) concentrations and local reactivation of circulating inert cortisone (11-dehydrocorticosterone in rodents) to cortisol (corticosterone) driven by 11␤-hydroxysteroid dehydrogenase type 1 (11␤-HSD-1) could play a pivotal role (4). However, the origins of the abovementioned dysregulations have not been established.Clinical and experimental evidence shows that the environment during the perinatal period plays an important role in the regulation of both metabolic and hormonal axes in adulthood. In humans, hyperglycemia and hyperinsulinemia in macrosomic fetuses of diabetic mothers were shown to favor later development of overweight (5). Conversely, it has been demonstrated that intrauterine g...

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Section: Methodsmentioning

confidence: 99%

Postnatal Diet-Induced Obesity in Rats Upregulates Systemic and Adipose Tissue Glucocorticoid Metabolism During Development and in Adulthood

et al. 2005

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“…Although shown to be an ACTH secretagogue, the physiologic role played by VP in the regulation of ACTH secretion is uncertain (3,19,20). Studies in Brattleboro rats, which genetically lack VP but have ACTH-releasing activity in extracts of their hypothalami and secrete ACTH in response to stress, suggest that VP plays only a minor role (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

“…Over the last decade, an hypothesis has emerged that VP may modulate the ACTH response to CRF and may be only one of several factors influencing ACTH secretion (3,19,23,24). Early studies showed that low doses of VP potentiated the ACTH-releasing activity of hypothalamic extracts in rats (25).…”

Section: Introductionmentioning

confidence: 99%

Arginine vasopressin potentiates adrenocorticotropin release induced by ovine corticotropin-releasing factor.

Debold¹,

Sheldon²,

DeCherney³

et al. 1984

J. Clin. Invest.

183

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A bstract. Arginine vasopressin (AVP) stimulates ACTH release in man and acts synergistically with synthetic ovine corticotropin-releasing factor (oCRF) in vitro. This study was designed to examine in man the combined effects of synthetic AVP (10 U intramuscularly) and oCRF (1 gg/kg intravenously) on ACTH release.Five normal male volunteers participated in five separate experiments: (a) AVP alone; (b) oCRF alone; (c) AVP followed by oCRF 15 min later; (d) simultaneous AVP and oCRF; and (e) insulin-induced hypoglycemia. Plasma immunoreactive ACTH (IR-ACTH) and IR-cortisol were measured for 4 h after injection of each hormone; basal levels for all subjects were .9±1.2 pg/ml and 4. 9±0.4 ,gg/dl (mean±SE), respectively. AVP and oCRF, when given individually, caused rapid rises in IR-ACTH to similar peak levels of 25±6.6 and 33±4.6 pg/ml, respectively. AVP given 15 min before oCRF caused a 2.6-fold potentiation ofthe oCRF response, with a peak IR-ACTH of 85±4.6 pg/ml. AVP given at the same time as oCRF produced a fourfold potentiation of the peak IR-ACTH response to 132±11 pg/ml. These ACTH responses were far greater than those previously observed after 30-fold greater doses of oCRF alone. By way of comparison, insulin-induced hypoglycemia caused a peak IR-ACTH of 169±20 pg/ml. IR-ACTH returned to base line at 60-90 min after AVP alone, whereas the prolonged effect of oCRF was apparent whether it was given alone or in combination with AVP. The mean peak IR-cortisol responses to AVP, oCRF, and AVP given 15 min before oCRF were similar (16.5±0.9, 16.4±2.3, and 18.5±0.8 ,ug/dl, respectively), but the peak IR-cortisol responses to AVP and oCRF given simultaneously and to insulininduced hypoglycemia were 1.5 and 1.7 times greater, respectively. IR-cortisol returned to base line within 2-3 h after AVP alone, but remained elevated for at least 4 h after oCRF alone or in combination with AVP. These results indicate that AVP acts synergistically with oCRF to release ACTH in man and suggest that AVP may play a physiologic role in modulating the ACTH response mediated by corticotropin-releasing factor.

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“…A spontaneous point mutation resulted in an altered AVP precursor which was unable to enter the secretory pathway (Evans et al, 2000, Surget andBelzung, 2008). As a result, homozygous AVP-deficient Brattleboro rats (KO) show diminished HPA axis responses to different acute stressors (Wiley et al, 1974, Conte-Devolx et al, 1982, Fink et al, 1992, accompanied by reduced depressive-and anxiety-like behavioral profile (Mlynarik et al, 2007). More specifically, AVP-deficient rats showed higher preference for a sweet solution, spent considerably shorter time immobile in the FS test and less time self-grooming on the elevated plus maze (EPM) accompanied by a higher level of dexamethasone-induced suppression of corticosterone response to restraint stress.…”

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confidence: 99%

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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Adrenocorticotropin,β-Endorphin, and Corticosterone Secretion in Brattleboro Rats*

Cited by 53 publications

References 0 publications

Postnatal Diet-Induced Obesity in Rats Upregulates Systemic and Adipose Tissue Glucocorticoid Metabolism During Development and in Adulthood

Postnatal Diet-Induced Obesity in Rats Upregulates Systemic and Adipose Tissue Glucocorticoid Metabolism During Development and in Adulthood

Arginine vasopressin potentiates adrenocorticotropin release induced by ovine corticotropin-releasing factor.

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

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