Hormonal effects on the neural retina: Corticoid uptake, specific binding and structural requirements for the induction of glutamine synthetase

Chader, Gerald J.; Reif‐Lehrer, Liane

doi:10.1016/0304-4165(72)90130-4

Cited by 50 publications

(19 citation statements)

References 17 publications

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“…The endogenous steroids, dehydroepiandrosterone (DHEA) and progesterone, have been shown to have antiglucocorticoid activity in several tissues, including the brain (Chader and Reif-Leher, 1972;Kaiser et al, 1979;Bohus and DeKloet, 1981;Giesen and Beck, 1982;Daynes et al, 1990;Blauer et al, 1991;Browne et al, 1992;Araneo et al, 1993). DHEA and progesterone exert antiglucocorticoid effects at the glucocorticoid type II receptor via mechanisms distinct from classical receptor antagonism (Chou and Luttge, 1998;Morfin and Starka, 2001), while progesterone acts as a classical antagonist at mineralocorticoid (type I glucocorticoid) receptors (reviewed in Turner, 1997).…”

Section: Introductionmentioning

confidence: 98%

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

Rasmusson

Vasek

Lipschitz

et al. 2004

Neuropsychopharmacol

122

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We recently found increased adrenal cortisol responses to adrenocorticotropic hormone (ACTH)1-24 and increased pituitary ACTH and adrenal cortisol responses to corticotropin-releasing factor in premenopausal women with chronic post-traumatic stress disorder (PTSD) compared to healthy nontraumatized subjects. This pattern of hypothalamic-pituitary-adrenal axis (HPA) hyper-reactivity has been previously seen in healthy individuals treated with the antiglucocorticoid mifepristone. We therefore investigated whether endogenous plasma levels of antiglucocorticoids such as dehydroepiandrosteroine (DHEA) and progesterone were increased in premenopausal women with PTSD at baseline or in response to adrenal activation by ACTH1-24. The study revealed that DHEA responses to 250 microg ACTH1-24 were increased in 13 PTSD subjects compared to 13 healthy nontraumatized subjects, while DHEA levels were generally increased in the PTSD subjects compared to seven healthy traumatized subjects. Cortisol responses to ACTH1-24 were also higher in the women with PTSD, while progesterone levels and responses were not different among the three groups. In addition, among the PTSD subjects, the peak change in DHEA in response to ACTH1-24 was negatively correlated with the total Clinician Administered PTSD Scale score, while the peak DHEA to cortisol ratio was inversely associated with negative mood symptoms measured by the Profile of Mood States scale. This work suggests that an increased capacity for DHEA release in response to extreme adrenal activation may influence the pattern of HPA axis adaptation to extreme stress, as well as mitigate the severity of PTSD and negative mood symptoms in premenopausal women with PTSD.

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Section: Introductionmentioning

confidence: 98%

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

Rasmusson

Vasek

Lipschitz

et al. 2004

Neuropsychopharmacol

122

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“…Interestingly, there is evidence that gonadal steroids, such as androgens, estrogens and gestagens are able to modulate the expression and activation of GR (for review on this see Turner, 1997) e.g. large concentrations of progesterone can block GR in chicken embryos (Chader and Reif-Lehrer, 1972). Henriksen et al (submitted for publication) found that female chickens (gallus gallus domesticus) with elevated plasma CORT levels deposit less androgens and gestagens in their eggs.…”

Section: Prenatal Hormone Exposure and Related Methological Issuesmentioning

confidence: 99%

Prenatal stress in birds: Pathways, effects, function and perspectives

Henriksen

Rettenbacher

Groothuis

2011

Neuroscience & Biobehavioral Reviews

181

147

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a b s t r a c tAlthough most work on prenatal stress has been conducted on mammalian species, birds provide useful alternative models since avian embryos develop outside the mother's body in a concealed environment, the egg, which is produced during a short time window of 4-14 days. This facilitates measurement of maternal substances provided for and manipulation of the embryo without interfering with the mother's physiology. We critically review prenatal corticosterone mediated effects in birds by reviewing both studies were females had elevated levels of plasma corticosterone during egg formation and studies applying corticosterone injections directly into the egg. A selected review of the mammalian literature is used as background. The results suggest that besides prenatal exposure to corticosterone itself, maternal corticosterone affects offspring's behaviour and physiology via alteration of other egg components. However, results are inconsistent, perhaps due to the interaction with variation in the post-natal environment, sex, age, developmental mode and details of treatment. The potential role of adaptive maternal programming has not been tested adequately and suggestions for future research are discussed.

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“…Both the glucocorticoid receptor Doglioni et al, 1990) are present in the -cells. However, it is known that progesterone may bind to the glucocorticoid receptor with an affinity similar to the natural glucocorticoids (Chader and Reif-Lehrer, 1972;Moguilewsky and Deraedt, 1981;Rupprecht et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Steroid effects on intracellular degradation of insulin and crinophagy in isolated pancreatic islets

Sandberg¹,

Borg²

2007

Molecular and Cellular Endocrinology

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Please cite this article as: Sandberg, M., Borg, L.A.H., Steroid effects on intracellular degradation of insulin and crinophagy in isolated pancreatic islets, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2007 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The effects of corticosterone and progesterone on intracellular degradation of insulin and crinophagy were determined in pancreatic -cells, and possible pathways mediating these effects were evaluated. Pancreatic islets were isolated from mice, intracellular degradation of insulin was measured by a pulse-chase method, and crinophagy was studied by electron microscopy. The islets were exposed to 3.3, 5.5 or 28 mM glucose with or without corticosterone, progesterone or the receptor ligands A-224817.0 and WAY-161358.Mifepristone was used to block steroid receptors and indomethacin to inhibit prostaglandin synthesis. Corticosterone caused a concentration-dependent decrease of insulin degradation at the lower glucose concentrations. Progesterone effected a concentration-dependent stimulation of insulin degradation. These results were paralleled with changes of the crinophagic activity in the -cells. Corticosterone decreased and progesterone increased islet production of prostaglandin E 2 . Mifepristone abolished the steroid actions on insulin degradation and prostaglandin production. The effects of corticosterone were mimicked by the selective glucocorticoid receptor modulator A-224817.0, but in contrast to progesterone, the selective progesterone receptor agonist WAY-161358 had no effect on insulin degradation or prostaglandin production. Inhibition of cyclooxygenase blocked insulin degradation. The findings indicate that both corticosterone and progesterone could affect intracellular insulin degradation and crinophagy solely via the glucocorticoid receptor, and that prostaglandins may have a regulatory role in intracellular turnover of secretory material in pancreatic islet -cells.

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Hormonal effects on the neural retina: Corticoid uptake, specific binding and structural requirements for the induction of glutamine synthetase

Cited by 50 publications

References 17 publications

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

An Increased Capacity for Adrenal DHEA Release is Associated with Decreased Avoidance and Negative Mood Symptoms in Women with PTSD

Prenatal stress in birds: Pathways, effects, function and perspectives

Steroid effects on intracellular degradation of insulin and crinophagy in isolated pancreatic islets

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