Localization and Specificity of Corticosteroid “Feedback Receptors” at the Hypothalamo-Hypophyseal Level; Comparative Effects of Various Steroids Implanted in the Median Eminence or the Anterior Pituitary of the Rat

Bohus, B.; Strashimirov, D

doi:10.1159/000121924

Cited by 25 publications

(6 citation statements)

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“…We have now shown that the CRF response of the hypothalamus to acetylcholine is altered by adrenalectomy and replacement therapy with corticosterone thus confirming our previous findings on the effect of electrical stimulation (Bradbury et al 1974). Our data, taken in conjunction with experi¬ ments on the implantation of corticosteroids in the hypothalamus (Smelik & Sawyer, 1962;Bohus & Strashimirov, 1970), lead us to conclude that this negative feedback effect of corticosteroids on the hypothalamus is of physiological significance.…”

Section: Discussionsupporting

confidence: 88%

Effect of Bilateral Adrenalectomy and Corticosteroid Therapy on the Secretion of Corticotrophin-Releasing Factor Activity From the Hypothalamus of the Rat in Vitro

Hillhouse¹,

Jones²

1976

Journal of Endocrinology

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The rat hypothalamus in vitro preparation was used to investigate the effect of bilateral adrenalectomy, with and without replacement therapy, on the release of corticotrophin-releasing factor(CRF). Corticotrophin-releasing factor was estimated using 48 h basal hypothalamic lesioned assay rats and corticosterone production of excised adrenals was used as the end point. Bilateral adrenalectomy resulted in depletion of hypothalamic CRF content within the first 2 h after the operation but this effect was prevented by replacement therapy with corticosterone. Thereafter, the hypothalamic CRF content returned to values not significantly different from the intact control level. Bilateral adrenalectomy caused an increase in both basal and acetylcholine-induced release of CRF and it is suggested that corticosteroids exert a negative feedback effect on the hypothalamus.

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Section: Discussionsupporting

confidence: 88%

Effect of Bilateral Adrenalectomy and Corticosteroid Therapy on the Secretion of Corticotrophin-Releasing Factor Activity From the Hypothalamus of the Rat in Vitro

Hillhouse¹,

Jones²

1976

Journal of Endocrinology

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“…However, the degree of inhibition of both parameters by cortisone was much less than that produced by dexamethasone. This compares with the relative potency of the two corticoids in the feedback suppression of ACTH release (30). The apparent differences in the effectiveness of the antagonism of estrogen-stimulated responses in the uterus by glucocorticoids and some sex steroids according to duration of pretreatment suggests possible differences in the mechanism(s) of inhibition or differing susceptibility to various steroid antagonists at similar points of inhibition.…”

Section: Discussionmentioning

confidence: 92%

The Mechanism of the Inhibition of Uterotrophic Responses by Acute Dexamethasone Pretreatment*

Campbell

1978

Endocrinology

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The mechanism of glucocorticoid antagonism of estradiol-stimulated uterotrophic responses was studied. Dexamethasone was administered sc at a dosage of 1000 /xg 20-25 min before an injection of 1 fig estradiol. Uterine weights were measured at 3 and 24 h, and the quantity of nuclear-bound receptor-estrogen complex (REC) was determined at 1 and 6 h using the nuclear exchange assay. Additionally, uteri were incubated in Eagle's medium containing 10~8 M [ 3 H]estradiol, either after an in vivo, or simultaneously with an in vitro, exposure to dexamethasone, and the quantity of nuclear-bound [ 3 H]estradiol and total tissue uptake of [ 3 H]estradiol were determined. Dexamethasone significantly reduced both 3-and 24-h uterine weights, with the early fluid imbibition being the more sensitive. This correlated with the dexamethasone-induced reduction in nuclear REC observed at 1 and 6 h after estradiol injection. Exposure of uteri either in vitro or in vivo to dexamethasone inhibited both nuclear bound and total tissue uptake of [ 3 H]estradiol in vitro. However, the reduction in total tissue uptake of [ 3 H]estradiol was greater than could be accounted for solely by the reduction in nuclear REC. Hence, it is proposed that dexamethasone acts to impair estrogen-induced growth of reproductive tissue indirectly. This impairment occurs at the level of the genome through reduction of nuclear REC as a result of restriction of transport of estradiol into uterine cells. Dexamethasone administration at various times after estradiol injection also reduced long term uterine growth. As dexamethasone antagonism of uterotrophic responses is evident even when the hormone is administered at times after the critical nuclear REC retention time necessary for eliciting long term growth, the reduction in nuclear REC is probably compounded by direct effects upon enzyme activity to impair uterine responsivity. (Endocrinology 103: 716, 1978)

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“…For example, adrenalectomy (ADX) results in higher PVN neuropeptide synthesis and secretion both at the basal and stressed states. Additionally, feedback can occur either directly at the level of the CRH and AVP neurons of the PVN as well as the corticotrophs of the anterior pituitary, or indirectly though GR and MR containing brain regions that project to the PVN such as the hippocampus and amygdala (Davidson and Feldman, 1967; Bohus and Strashimirov, 1970; Dallman et al, 1987; Sawchenko, 1987). Glucocorticoid effects vary according to duration of exposure.…”

Section: Discussionmentioning

confidence: 99%

Estrogen impairs glucocorticoid dependent negative feedback on the hypothalamic–pituitary–adrenal axis via estrogen receptor alpha within the hypothalamus

2009

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Numerous studies have established a link between individuals with affective disorders and a dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, most notably characterized by a reduced sensitivity to glucocorticoid negative (−) feedback. Furthermore there is a sex difference in the etiology of mood disorders with incidence in females being two to three times that of males, an association that may be a result of the influence of estradiol (E2) on HPA axis function. In these studies, we have examined the effect of E2 on glucocorticoid-mediated HPA axis (−) feedback during both the diurnal peak and the stress-induced rise in corticosterone (CORT). Young adult female Sprague–Dawley (SD) rats were ovariectomized (OVX) and 1 week later treated subcutaneous (s.c.) with oil or estradiol benzoate (EB) for 4 days. On the 4th day of treatment, animals were injected with a single dose of dexamethasone (DEX), or vehicle. EB treatment significantly increased the evening elevation in CORT and the stress-induced rise in CORT. In contrast, DEX treatment reduced the diurnal and stress induced rise in CORT and adrenocorticotropic hormone (ACTH), and this reduction was not apparent following co-treatment with EB. To determine a potential site of E2’s action, female SD rats were OVX and 1 week later, wax pellets containing E2, the estrogen receptor beta (ERβ) agonist diarylpropionitrile (DPN), or the estrogen receptor alpha (ERα) agonist propylpyrazoletriol (PPT), was implanted bilaterally and dorsal to the paraventricular nucleus of the hypothalamus (PVN). Seven days later, animals were injected s.c. with a single dose of DEX, or vehicle to test for glucocorticoid-dependent (−) feedback. Results show that E2 and PPT increased, while DPN decreased the diurnal peak and stress-induced CORT and ACTH levels as compared to controls. Furthermore, E2 and PPT impaired the ability of DEX to inhibit both the diurnal and the stress-induced rise in CORT and ACTH, whereas DPN had no effect. Neuronal activation was measured by c-fos mRNA expression within the PVN following restraint. E2 and PPT increased c-fos mRNA, and impaired the normal DEX suppression of neuronal activation in the PVN. Taken together, these data indicate that estradiol causes a dysregulation of HPA axis (−) feedback as evidenced by the inability of DEX to suppress diurnal and stress-induced CORT and ACTH secretion. Additionally, the ability of E2 to inhibit glucocorticoid (−) feedback occurs specifically via ERα acting at the level of the PVN.

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Localization and Specificity of Corticosteroid “Feedback Receptors” at the Hypothalamo-Hypophyseal Level; Comparative Effects of Various Steroids Implanted in the Median Eminence or the Anterior Pituitary of the Rat

Cited by 25 publications

References 1 publication

Effect of Bilateral Adrenalectomy and Corticosteroid Therapy on the Secretion of Corticotrophin-Releasing Factor Activity From the Hypothalamus of the Rat in Vitro

Effect of Bilateral Adrenalectomy and Corticosteroid Therapy on the Secretion of Corticotrophin-Releasing Factor Activity From the Hypothalamus of the Rat in Vitro

The Mechanism of the Inhibition of Uterotrophic Responses by Acute Dexamethasone Pretreatment*

Estrogen impairs glucocorticoid dependent negative feedback on the hypothalamic–pituitary–adrenal axis via estrogen receptor alpha within the hypothalamus

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