The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform
M Le Moal - One of the best experts on this subject based on the ideXlab platform.
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Hippocampal type I and type II corticosteroid Receptors are modulated by central noradrenergic systems.
Psychoneuroendocrinology, 1992Co-Authors: S Maccari, P Mormède, P V Piazza, H Simon, L Angelucci, M Le MoalAbstract:The effects of corticosteroids on various brain functions, including the negative feedback control of hypothalamo-pituitary-adrenal (HPA) axis activity, are mediated by two types of Receptors (type I, or mineralocorticoid, and type II, or glucocorticoid) in the central nervous system. Although receptor numbers are thought to be regulated by circulating levels of Corticosterone, there may be a direct neural control of corticosteroid Receptors. In the present experiments, we demonstrate that 6-OHDA lesioning of noradrenergic (NA) ascending pathways in the pedunculus cerebellaris superior (PCS) reduces Corticosterone secretion in response to novelty and increases the number of hippocampal type I corticosteroid Receptors in rats 24 hr after adrenalectomy. The same lesion in adrenalectomized animals in which Corticosterone levels were maintained within normal limits by Corticosterone replacement implants also led to an increase in the number of type I Corticosterone Receptors and a decrease in the apparent affinity (Kd) of type II Receptors in the hippocampus. These results suggest that the NA system may regulate HPA axis activity via a direct control of the number of type I Receptors and the apparent affinity of type II Receptors in the hippocampus. The possibility that there is a neural control of corticosteroid Receptors may throw light on mechanisms controlling HPA axis activity and may suggest other approaches to the treatment of dysregulation of the HPA axis observed during stress and in certain psychopathological conditions.
S Maccari - One of the best experts on this subject based on the ideXlab platform.
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Hippocampal type I and type II corticosteroid Receptors are modulated by central noradrenergic systems.
Psychoneuroendocrinology, 1992Co-Authors: S Maccari, P Mormède, P V Piazza, H Simon, L Angelucci, M Le MoalAbstract:The effects of corticosteroids on various brain functions, including the negative feedback control of hypothalamo-pituitary-adrenal (HPA) axis activity, are mediated by two types of Receptors (type I, or mineralocorticoid, and type II, or glucocorticoid) in the central nervous system. Although receptor numbers are thought to be regulated by circulating levels of Corticosterone, there may be a direct neural control of corticosteroid Receptors. In the present experiments, we demonstrate that 6-OHDA lesioning of noradrenergic (NA) ascending pathways in the pedunculus cerebellaris superior (PCS) reduces Corticosterone secretion in response to novelty and increases the number of hippocampal type I corticosteroid Receptors in rats 24 hr after adrenalectomy. The same lesion in adrenalectomized animals in which Corticosterone levels were maintained within normal limits by Corticosterone replacement implants also led to an increase in the number of type I Corticosterone Receptors and a decrease in the apparent affinity (Kd) of type II Receptors in the hippocampus. These results suggest that the NA system may regulate HPA axis activity via a direct control of the number of type I Receptors and the apparent affinity of type II Receptors in the hippocampus. The possibility that there is a neural control of corticosteroid Receptors may throw light on mechanisms controlling HPA axis activity and may suggest other approaches to the treatment of dysregulation of the HPA axis observed during stress and in certain psychopathological conditions.
Efthimia Kitraki - One of the best experts on this subject based on the ideXlab platform.
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Contribution of sex and cellular context in the regulation of brain corticosteroid Receptors following restraint stress.
Neuroendocrinology, 2000Co-Authors: Despoina Karandrea, Christos Kittas, Efthimia KitrakiAbstract:The two subtypes of Corticosterone Receptors in the rat brain play a pivotal role in the modulation of the stress response. Appropriate control of their gene expression is therefore critical for the maintenance of cellular and organism homeostasis. In this study, we investigated the contribution of gender and of the cellular environment of certain brain areas to the expression of both types of corticosteroid Receptors, following restraint stress. Adult Wistar rats of both sexes were subjected to acute, chronic or to a combined chronic plus acute stress regimen, and the expression of glucocorticoid and mineralocorticoid Receptors was evaluated in their hippocampus, hypothalamus, pituitary and frontal cortex, by using Northern blot analysis. Significant sex differences were observed in the first three brain areas examined as to the stress-induced expression of corticosteroid Receptors. Among these, females showed a distinct mechanism of regulating glucocorticoid/mineralocorticoid receptor ratio in the hippocampus upon chronic stress, while the female hypothalamus was more prone than the male to changing corticosteroid receptor expression in response to restraint stress. In another set of experiments, we assessed the influence of ovarian steroids on stress-induced corticosteroid receptor expression in the above brain areas by analyzing ovariectomized rats exposed to short-term restraint. Our results showed that although ovarian steroids affect the stress-induced expression of receptor genes in a region-specific manner, their elimination does not appear to lead to the male pattern of expression. These findings provide further evidence for the existence of both regional and gender specificity in the regulation of brain and pituitary corticosteroid Receptors following stress, and support the hypothesis of a distinct male and female neuroendocrine axis in response to stress.
R. D. Stith - One of the best experts on this subject based on the ideXlab platform.
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Relative contribution of type I and II Corticosterone Receptors in VMH lesion-induced obesity and hyperinsulinemia
American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 1994Co-Authors: Terrie Thomas, Lynn D. Devenport, R. D. StithAbstract:Ventromedial hypothalamic (VMH) lesion-induced obesity is accompanied by hyperinsulinemia and hyperphagia, which are dependent upon Corticosterone (Cort) for their expression. Whether Cort exerts these actions through its stimulation of type I or II Cort receptor populations is unknown. Therefore, food intake and weight gain were measured in obese adrenalectomized VMH-lesioned rats given continuous infusion of various doses of either a type I-receptor agonist (aldosterone), a type II-receptor agonist (RU-28362), or several combination doses. Similarly, the receptor population responsible for lesion-induced hyperinsulinemia was identified. Type II receptor stimulation restored the hyperphagia, weight gain, and hyperinsulinemia of adrenalectomized VMH-lesioned animals, while type I receptor stimulation blocked their weight loss.
Kjell Fuxe - One of the best experts on this subject based on the ideXlab platform.
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Prenatal Corticosterone increases spontaneous and d-amphetamine induced locomotor activity and brain dopamine metabolism in prepubertal male and female rats
Neuroscience, 1995Co-Authors: Rochellys Diaz, Sven-ove Ögren, Mariann Blum, Kjell FuxeAbstract:Abstract Recently, both glucocorticoid receptor immunoreactivity and glucocorticoid receptor messenger RNA levels were found in multiple brain areas, especially in the neuroepithelium during the late prenatal development of the rat brain. To better understand the potential influence of stress on fetal brain development by release of maternal adrenocortical steroids, we have investigated the effects of Corticosterone administration to pregnant rats on the locomotor activity of their prepubertal offspring. On day 16 of pregnancy female rats were implanted with either placebo or Corticosterone pellets (release of 2.4 mg/day for seven days). After birth their offspring were nursed by foster mothers to avoid any postnatal effects of the Corticosterone pellets. At three weeks of age, the offspring were tested for spontaneous motor behaviours. Both male and female offspring from Corticosterone treated mothers showed significantly increased spontaneous ambulation, motility and rearing compared to placebo treated groups. No significant sex differences were found in locomotor activity between male and female offspring from placebo groups. Following d-amphetamine (1.5 mg/kg) treatment, a prefential dopamine releasing agent, we observed a significant increase in ambulation, motility and rearing activity in the male offspring treated with Corticosterone. In the female offspring, only the rearing activity was significantly higher after d-amphetamine treatment in the prenatal Corticosterone group compared with the placebo treated group. Basal dopamine metabolism (dihydroxyphenylacetic acid/dopamine ratio) was increased in the dorsal striatum and ventral striatum of male and female offspring from Corticosterone-treated dams. In the male offspring, Corticosterone treatment was associated with a disappearance of the right side dominance of dopamine metabolism in the dorsal striatum. These results suggest that prenatal administration of Corticosterone in low physiological doses can affect the postnatal development of spontaneous locomotor activity and dopamine function in a manner which is partly different in the two sexes. The effects observed may be mediated by direct activation of Corticosterone Receptors in the fetal brain.
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Corticosterone treatment counteracts lesions induced by neonatal treatment with monosodium glutamate in the mediobasal hypothalamus of the male rat.
Neuroscience letters, 1991Co-Authors: Michele Zoli, Francesco Ferraguti, Giuseppe Biagini, Antonio Cintra, Kjell Fuxe, Luigi F. AgnatiAbstract:Abstract The effects of glucocorticoids on monosodium glutamate-induced neurotoxicity in the neonatal basal hypothalamus were studied by means of semiquantitative immunocytochemistry for tyrosine hydroxylase, growth hormone releasing factor and luteinizing hormone releasing hormone. Neonatal monosodium glutamate treatment induced a marked decrease in tyrosine hydroxylase immunoreactive neurons in the arcuate nucleus and growth hormone releasing factor immunoreactive nerve terminals in the median eminence. These effects were significantly antagonized by the coad-ministration of Corticosterone. Corticosterone alone had no effect on the parameters studied. No significant change in luteinizing hormone releasing hormone immunoreactivity in the median eminence was detected after any treatment. These results demonstrate that Corticosterone, possibly acting via type II Corticosterone Receptors which are highly enriched in the arcuate neurons, can exert a protective action on glutamate-induced neurotoxicity.
