1991
DOI: 10.1016/0960-0760(91)90172-2
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Central peptidergic neurons as targets for glucocorticoid action. Evidence for the presence of glucocorticoid receptor immunoreactivity in various types of classes of peptidergic neurons

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Cited by 83 publications
(35 citation statements)
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“…The results obtained during TRH stimulation indicate a cortisol-mediated change in the density of TRHreceptors on the thyrotrophs, which may occur within a few hours (41). Our results do not exclude that this effect may be amplified by an inhibition of TRH release (42,43), and glucocorticoid-receptors have been demonstrated on all the paraventricular TRH neurons (44). In the present study, serum T 3 levels increased significantly during hypocortisolism, and the apparently inappropriate increase in TSH, despite an elevated serum T 3 concentration, favor a centrally mediated effect.…”
Section: Discussionsupporting
confidence: 46%
“…The results obtained during TRH stimulation indicate a cortisol-mediated change in the density of TRHreceptors on the thyrotrophs, which may occur within a few hours (41). Our results do not exclude that this effect may be amplified by an inhibition of TRH release (42,43), and glucocorticoid-receptors have been demonstrated on all the paraventricular TRH neurons (44). In the present study, serum T 3 levels increased significantly during hypocortisolism, and the apparently inappropriate increase in TSH, despite an elevated serum T 3 concentration, favor a centrally mediated effect.…”
Section: Discussionsupporting
confidence: 46%
“…It has been suggested that plasma corticosterone is implicated in the hypothalamic NPY expression. [18][19][20][21] Taken together, it is concluded that a chronic increase in plasma corticosterone in MS/RF rats during the repeated fasting/RF cycles might have contributed to a tonic increase in NPY expression, and the increased plasma corticosterone and NPY expression by repeated fasting/RF cycles may partly be in charge of the sustained compensatory hyperphagia in the MS/RF group. Previous reports have suggested that elevated plasma corticosterone may be necessary for fasting-induced increase in NPY mRNA expression.…”
Section: Discussionmentioning
confidence: 99%
“…13,14 NPY, a potent orexic peptide, stimulates feeding. [15][16][17] Several results suggest that glucocorticoids regulate the hypothalamic NPY expression: adrenalectomy downregulates the expression of NPY gene in the hypothalamus; 18 NPY neurons in the hypothalamic arcuate nucleus contain glucocorticoid receptors 19 and elevated plasma corticosterone appears to be necessary for fastinginduced increase in NPY mRNA expression. 20,21 These reports led us to hypothesize that neonatal MS may lead to development of eating disorders in the offspring later in life, possibly, due to altered HPA axis characteristics modulating the hypothalamic expression of feeding peptides.…”
Section: Introductionmentioning
confidence: 99%
“…There is a GC response element upstream of the rat NPY gene, and GC receptors have been shown to be highly expressed in all NPY-containing neurons in the arcuate nucleus (33)(34)(35). Since all arcuate AGRP neurons express NPY, there are GC receptors in AGRP neurons (11).…”
Section: Discussionmentioning
confidence: 99%