17α-Alkynyl-11β,17-dihydroxyandrostane derivatives : A new class of potent glucocorticoids.

Teutsch, G.; Costerousse, G.; Deraedt, R.; Benzoni, J.; Fortin, Marc; Philibert, D.

doi:10.1016/0039-128x(81)90084-2

Cited by 98 publications

(31 citation statements)

References 8 publications

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“…These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC. Although treatment with RU 28362 induces a selective activation of GRs (32), there is extensive evidence that exposure to a mild stressor or systemic administration of corticosterone or cortisol induces comparable enhancement of memory consolidation (18,33,34) or impairment of working memory in rats, monkeys, and humans (1, 9). However, it should be noted that the influences of stress and glucocorticoids on both working memory and memory consolidation follow an inverted-U-shaped doseresponse relationship and vary with the severity of the stressor, drug dosage, or other experimental conditions (9,(33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

“…The specific GR agonist RU 28362 (11β,17β-dihydroxy-6,21-dimethyl-17α-pregna-4,6-trien-20yn-3-one, 3 or 10 ng in 0.5 μL; a gift from Aventis) was infused into the mPFC either alone or together with the specific β 1 -adrenoceptor antagonist atenolol (1.25 μg; Sigma-Aldrich), the specific α 1 -adrenoceptor antagonist urapidil (0.3 μg; Sigma-Aldrich), the cAMP inhibitor Rp-cAMPS (10 μg; Sigma-Aldrich), or the cell-permeable PKA inhibitor PKI 14-22 amide (0.3 μg; Calbiochem). Receptor binding studies have shown that RU 28362 has selective and high affinity for GRs (32). Drugs were first dissolved in 100% ethanol and subsequently diluted in 0.9% saline to reach a final ethanol concentration of 0.5%.…”

Section: Methodsmentioning

confidence: 99%

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Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

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

234

169

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It is well established that acute administration of adrenocortical hormones enhances the consolidation of memories of emotional experiences and, concurrently, impairs working memory. These different glucocorticoid effects on these two memory functions have generally been considered to be independently regulated processes. Here we report that a glucocorticoid receptor agonist administered into the medial prefrontal cortex (mPFC) of male Sprague-Dawley rats both enhances memory consolidation and impairs working memory. Both memory effects are mediated by activation of a membrane-bound steroid receptor and depend on noradrenergic activity within the mPFC to increase levels of cAMPdependent protein kinase. These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

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

234

169

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“…The synthetic steroid. RU 26988, which has been reported to have only glucocorticoid effects (Teutsch et al, 1981). also caused a dosedependent decrease in CAT and increase in TH activities with a maximal effect at 10"' M (Fig.…”

Section: Responses To Corticosterone Aidosterone and Rv 26988mentioning

confidence: 88%

Pharmacology of the Steroid Regulation of Transmitter Choice in Cultured Rat Sympathetic Ganglia

McLennan

Hill

Hendry

1984

Aust J Exp Biol Med

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Summary. The normally adrenergic rat superior cervical ganglion becomes cholinergic when grown in explant culture. This response is prevented by the physiological glucocorticosteroid, corticosterone, and the mineralocorticoid, aldosterone. The synthetic glucocorticosteroid. RU 26988, was also active in this respect. Progesterone, spironolactone, testosterone and 173-estradiol were all inactive at 10-*" M, demonstrating the specificity of the response. The response to 10-' M corticosterone was not antagonized by a hundred-fold excess of progesterone, testosterone, cortexolone or spironolactone. The response to 10-'M aldosterone was antagonized by spironolactone but not by progesterone.The order of potency of the agonists in this study is similar to that described for classical glucocorticoid receptors. TTie action of aldosterone was antagonized, however, by the mineralocorticoid antagonist, spironolactone. Thus, the steroid response described here may be mediated by both gtucocorticoid and mineralocorticoid receptor? or, alternatively, by a new glucocorticoid receptor which can be antagonized by a mineralocorticoid antagonist.

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“…The 10 nmol/100 g body weight twice-daily dose has been demonstrated to markedly increase cation transport in adrenalectomized rat colon (1). To determine the maximal colonic response to glucocorticoid in the absence of crossover binding to the aldosterone receptor, we gave adrenalectomized rats RU26988 (Roussel UCLAF, France), a highly specific synthetic glucocorticoid with virtually no binding to the aldosterone receptor or to plasma corticosterone-binding globulin (23,24). The steroid was administere in twice-daily doses of 5, 15, 30, and 60 nmol/100 g body wt.…”

Section: Methodsmentioning

confidence: 99%

“…The steroid was administere in twice-daily doses of 5, 15, 30, and 60 nmol/100 g body wt. Because RU26988's affinity for the glucocorticoid receptor is as high or higher than that of dexamethasone, the higher doses should saturate the glucocorticoid receptor (23)(24)(25). We have demonstrated that this steroid has potent agonist activities in colon (10 …”

Section: Methodsmentioning

confidence: 99%

Regulation of cation transport by low doses of glucocorticoids in in vivo adrenalectomized rat colon.

Bastl¹

1987

J. Clin. Invest.

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A dose response curve for glucocorticoid-induced proximal and distal colonic cation transport in vivo was established in adrenalectomized rats. All doses (0.5-50 nmol/100 g body wt) stimulated sodium absorption. Distal sodium absorption did not saturate at dexamethasone levels that saturate the glucocorticoid receptor but also bind to > 35% of aldosterone receptors. Saturation of the pure glucocorticoid response occurred in both segments with RU26988, a synthetic glucocorticoid that does not occupy aldosterone receptors. Maximum velocities for pure glucocorticoid-induced sodium absorption were 15 and 16 teq/min per g dry tissue, and Michaelis constants (K.) were 4.2 and 4.6 X 10-' mol/liter for proximal and distal colon. Ks are similar to the dissociation constant for the colonic glucocorticoid receptor and too low for significant aldosterone receptor occupancy. Dexamethasone increased sodium absorption significantly within 30 min of injection, suggesting the response is not dependent on new protein synthesis. Similar time and dose responses in proximal and distal colon suggest glucocorticoids stimulate the same pathway in both segments.

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17α-Alkynyl-11β,17-dihydroxyandrostane derivatives : A new class of potent glucocorticoids.

Cited by 98 publications

References 8 publications

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Pharmacology of the Steroid Regulation of Transmitter Choice in Cultured Rat Sympathetic Ganglia

Regulation of cation transport by low doses of glucocorticoids in in vivo adrenalectomized rat colon.

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