Caffeine Enhances the Speed of the Recovery of the Hypothalamo-Pituitary-Adrenocortical Axis after Chronic Prednisolone Administration in the Rat

Marzouk, H.; Zuyderwijk, J.; Uitterlinden, Piet; Koetsveld, Peter van; Blijd, J.; Abou-Hashim, E. M.; El-Kannishy, Mohammed H.; Jong, Frank H. de; Lamberts, Steven W. J.

doi:10.1159/000125932

Cited by 12 publications

(5 citation statements)

References 13 publications

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“…The FST is primarily associated with the dopaminergic and serotonergic systems, while the TST is associated with the adrenergic system (Martin and Brown 2009). Our findings that the stress-induced increase in plasma corticosterone and ACTH concentrations are suppressed by the administration of clomipramine are in line with other authors' results (Aulakh et al 1993;Martin and Brown 2009;Marzouk et al 1991). Placebo analgesia also decreased the stress-induced corticosterone and ACTH concentrations.…”

Section: Discussionsupporting

confidence: 92%

Placebo analgesia affects the behavioral despair tests and hormonal secretions in mice

et al. 2011

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Section: Discussionsupporting

confidence: 92%

Placebo analgesia affects the behavioral despair tests and hormonal secretions in mice

et al. 2011

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“…[54] have demonstrated that rats implanted to moderately in crease basal a.m. corticosterone show normal ACTH but depressed plasma corticosterone responses to stress in the p.m. In addition, dispersed adrenal cells, from rats treated with corticosteroids in vivo, have been shown to secrete less corticosterone in response to ACTH challenge [55]. It must be noted however that animals bom by C section with no added anoxia (0-min anoxia group) showed no change in basal corticosterone secretion, but still hyposecreted corticosterone in response to stress.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal and Hypothalamic Type I Corticosteroid Receptor Affinities Are Reduced in Adult Rats Born by a Caesarean Procedure with or without an Added Period of Anoxia

Boksa

Krishnamurthy²,

Sharma³

1996

Neuroendocrinology

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Brief periods of hypoxia during labour and birth are a frequent occurrence. Within the CNS, the hippocampus is known to be particularly vulnerable to the damaging effects of hypoxia/ischaemia in both adult and immature animals. The hippocampus also contains the highest concentration of corticosteroid receptors of any brain region and both mineralocorticoid (type I) receptors and glucocorticoid (type II) receptors in the hippocampus play a role in the regulation of basal diurnal and stress-induced glucocorticoid secretion. Given this background, the aim of this study was to test whether an acute period of anoxia during the birth process may have lasting effects on CNS corticosteroid receptor levels and/or pituitary-adrenocortical function. Type I and type II corticosteroid receptor binding sites in the hippocampus and hypothalamus were compared in adult rats that had been born vaginally, born by a Caesarean procedure or born by a Caesarean procedure with 5,10 or 15 min of added anoxia. Using 14 nM [³H]corticosterone as radioligand, mineralocorticoid receptor binding was reduced by approximately 50% in the hippocampus and hypothalamus of adult rats that had been born by the Caesarean procedure either with or without an added period of anoxia, in comparison to vaginally born controls. Saturation analysis revealed that these reductions resulted from decreases in affinity of the mineralocorticoid receptor for [³H]corticosterone, with no change in numbers of receptors. Birth condition had no effect on glucocorticoid receptor binding capacities in the hippocampus or hypothalamus. A small increase in basal corticosterone secretion during the diurnal trough was observed in adult animals that had been born by Caesarean section with 5 or 15 min of added anoxia. The plasma corticosterone response to a 20-min restraint stress was reduced in adult animals born by Caesarean section with or without an added period of anoxia, in comparison to vagmally born controls. However the adrenocorticotropin response to stress was largely unaffected by birth condition. The results indicate that an acute birth insult is sufficient to produce long-lasting alterations in hippocampal and hypothalamic mineralocorticoid receptor sites, accompanied by changes in basal and stress-induced glucocorticoid secretion.

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“…A similar procedure was followed to measure plasma free T3 (FT-,). Corticosterone was esti¬ mated by RIA (Marzouk et al 1991). Detection limits were 02 µg RP-2 TSH/1, 2 nmol T4/l, 01 nmol T3/l and 1 nmol corticosterone/1.…”

Section: Hormone Determinationsmentioning

confidence: 99%

Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland

Haasteren¹,

Linkels²,

Klootwijk³

et al. 1995

Journal of Endocrinology

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The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160-169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSH beta mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160-169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160-169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that alpha-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0.2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSH beta mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone.

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Caffeine Enhances the Speed of the Recovery of the Hypothalamo-Pituitary-Adrenocortical Axis after Chronic Prednisolone Administration in the Rat

Cited by 12 publications

References 13 publications

Placebo analgesia affects the behavioral despair tests and hormonal secretions in mice

Placebo analgesia affects the behavioral despair tests and hormonal secretions in mice

Hippocampal and Hypothalamic Type I Corticosteroid Receptor Affinities Are Reduced in Adult Rats Born by a Caesarean Procedure with or without an Added Period of Anoxia

Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland

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