ACTH content in the anterior pituitary after the infusion of various doses of corticosterone and dexamethasone in normal and adrenalectomized rats.

Sakakura, Muneki; Yoshioka, Mitsuaki; Kobayashi, Masashi

doi:10.1620/tjem.137.191

Cited by 5 publications

(7 citation statements)

References 9 publications

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“…This is an important finding because it implies that the alteration we observed in hypothalamic ACTH was specific and not due to a generalized effect of dexamethasone to increase neuronal content of hypotha lamic neuropeptides. Previous studies have reported an in crease [2], decrease [15,24], or no change [33] in hypotha lamic CRH content with dexamethasone. Methodologic differences in these studies make valid comparison diffi cult.…”

Section: Discussionmentioning

confidence: 82%

“…Although tissue content studies may be difficult to interpret due to the dynamic relationship be tween synthesis and release, the present findings of in creased hypothalamic tissue ACTH content coupled with decreased CSF ACTH suggest that dexamethasone inhibits release of immunoreactive ACTH from hypothalamic AC'TH-containing neurons. Dexamethasone has previously been shown to inhibit release of ACTH from the anterior pituitary corticotroph both in vitro [4,9,30] and in vivo [24]. While its effect on peripheral ACTH release is primarily at the level of the pituitary [23], dexamethasone does cross the blood-brain barrier and can bind to specific steroid binding sites in the brain [3,23].…”

Section: Discussionmentioning

confidence: 99%

“…78% for ACTH . and I I7% for ACTH (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). By increasing the duration of the incubations at each step, the amount of ACTH required to reduce trace binding by I0% (EDio) is 0.25 pg/tube, with half-maximal displacement of tracer at 2.6 pg/tube.…”

Section: Tissue Extractionmentioning

confidence: 99%

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Effects of Dexamethasone on Central and Peripheral ACTH Systems in the Rat

et al. 1987

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To investigate the simultaneous effects of dexamethasone on peripheral and central adrenocorticotropic hormone (ACTH) systems, rats were treated with dexamethasone or saline for 4 days. Pituitary, plasma, hypothalamus and cerebrospinal fluid (CSF) were then collected and analyzed for ACTH immunoreactivity. Additionally, hypothalamic tissue extracts were analyzed for corticotropin-releasing hormone (CRH) immunoreactivity. Dexamethasone significantly lowered peripheral levels of ACTH as measured in pituitary and plasma. Hypothalamic ACTH content significantly increased while CSF ACTH significantly decreased with dexamethasone treatment. Hypothalamic CRH concentrations showed a small but statistically insignificant decrease. These results (1) suggest that prolonged exposure to dexamethasone affects central as well as peripheral ACTH activity, (2) corroborate our previous findings in rhesus monkeys of decreased CSF ACTH in response to prolonged dexamethasone treatment, (3) suggest that dexamethasone may inhibit the release of ACTH from hypothalamic neurons into the CSF, and (4) provide evidence that the effect of dexamethasone on pituitary ACTH content is of greater magnitude than its effect on hypothalamic CRH.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

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Effects of Dexamethasone on Central and Peripheral ACTH Systems in the Rat

et al. 1987

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“…An increase in FKBP51, induced by GC via an ultra-short feedback loop, reduces sensitivity and in turn nuclear translocation of the receptor (for review see [29]). At the level of the pituitary, GC exert their negative feedback function by repressing the gene encoding for pro-opiomelanocortin (POMC), the precursor of ACTH [30], by directly inhibiting the release of ACTH vesicles into the periphery [31], [32] or by reducing CRH-R1 binding [33].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Underlying the Increased Plasma ACTH Levels in Chronic Psychosocially Stressed Male Mice

2013

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Mice exposed to chronic subordinate colony housing (CSC, 19 days), an established paradigm for chronic psychosocial stress, show unaffected basal morning plasma corticosterone (CORT) concentrations, despite enlarged adrenal glands and an increased CORT response to an acute heterotypic stressor. In the present study we investigate the mechanisms underlying these phenomena at the level of the pituitary. We show that both basal and acute stressor-induced (forced swim (FS), 6 min) plasma adrenocorticotropic hormone (ACTH) concentrations, the number of total and corticotroph pituitary cells, and relative protein expression of pituitary mineralocorticoid receptor and FK506-binding protein 51 was increased in CSC compared with single-housed control (SHC) mice, while relative corticotropin releasing hormone (CRH) receptor 1 (CRH-R1) and glucocorticoid receptor protein expression was down-regulated. Relative pituitary pro-opiomelanocortin and arginine vasopressin (AVP) receptor 1b (AVPR-1b) protein expression, FS (6 min)-induced ACTH secretion in dexamethasone-blocked mice, and the number of AVP positive magnocellular and parvocellular neurons in the paraventricular hypothalamic nucleus (PVN) was unaffected following CSC. Taken together, the data of the present study indicate that 19 days of CSC result in pituitary hyperactivity, under both basal and acute heterotypic stress conditions. Although further studies have to assess this in detail, an increased number of pituitary corticotrophs together with unaffected relative pituitary AVPR-1b and decreased CRH-R1 protein expression following CSC suggests that pituitary hyperdrive is mediated by newly formed corticotrophs that are more sensitive to AVP than CRH. Moreover, our data indicate that changes in PVN AVP and negative feedback inhibition seem not to play a major role in pituitary hyperactivity following CSC.

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“…Upon disruption of cortisol synthesis, cortisol concentrations diminish slowly (τ ∼ 1hr) CRH concentrations rises abruptly (and probably in stages) after more than 1 hour of delay [5]; while the authors suggest a rate-sensitive feedback, the observed profiles suggest that a threshold (and probably multiple threshold) mechanism, relative to a set point, is more plausible. Constant infusion of a relatively small dose of 20 micrograms dexamethasone (DEX) did not reduce the hypothalamic CRF content; in contrast, the infusion of 202 and 504 micrograms DEX over 6 hr significantly reduced the hypothalamic CRF content [142]. These two evidences suggest a threshold mechanism for CRH synthesis regulation by GC.…”

Section: Ppvn-crhmentioning

confidence: 94%

A Hierarchical Model of the Hypothalamo-Adreno-Pituitary system

Rota

Vuza

Climescu-Haulica

2019

Preprint

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We present a model of the Hypothalamo-Adreno-Pituitary (HPA) system; our approach is hierarchical and biologically sound, reflecting the complexity of the real HPA system. The structure of the conceptual model is based on theoretical frameworks of biological complex systems and its implementation takes advantage of recent hybrid automata modelling and analysis tools, being modular and reflecting parameter and mechanisms uncertainties.

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ACTH content in the anterior pituitary after the infusion of various doses of corticosterone and dexamethasone in normal and adrenalectomized rats.

Cited by 5 publications

References 9 publications

Effects of Dexamethasone on Central and Peripheral ACTH Systems in the Rat

Effects of Dexamethasone on Central and Peripheral ACTH Systems in the Rat

Mechanisms Underlying the Increased Plasma ACTH Levels in Chronic Psychosocially Stressed Male Mice

A Hierarchical Model of the Hypothalamo-Adreno-Pituitary system

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