Publications by authors named "Murphy-Weinberg V"

Using a longitudinal approach, we sought to define the interplay between genetic and nongenetic factors in shaping vulnerability or resilience to COVID-19 pandemic stress, as indexed by the emergence of symptoms of depression and/or anxiety. University of Michigan freshmen were characterized at baseline using multiple psychological instruments. Subjects were genotyped, and a polygenic risk score for depression (MDD-PRS) was calculated.

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Background: Negative feedback regulation of the hypothalamic-pituitary-adrenal axis occurs through a dual-receptor system of mineralocorticoid receptors (MR) and glucocorticoid receptors (GR). Their affinity for cortisol and their distribution in the brain differ. Studies using an MR antagonist have demonstrated that MR is active throughout the circadian rhythm.

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In patients with major depression, abnormalities in baseline cortisol secretion and resistance to negative feedback are well established. However, it is unclear if patients with major depression have alterations in the hypothalamic-pituitary-adrenal (HPA) response to stressors. While other challenges to the HPA axis have used endocrine stimuli such as insulin-induced hypoglycemia, we now report of the response to a social stressor in patients with major depression and matched control subjects.

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In rodents, two types of glucocorticoid receptors, the mineralocorticoid (MR; type I) and the glucocorticoid (type II) receptors, have been demonstrated to play a role in hypothalamic-pituitary-adrenal (HPA) axis regulation. Because MR shows a very high affinity for cortisol, it has been suggested that MR plays an important role in restraint of CRH and ACTH secretion during the nadir of the circadian rhythm. Although a number of studies have established the importance of MR in rodents, the functional role of MR in humans has not been determined.

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Excess secretion of cortisol in depressed patients has been documented by a number of investigators, which is presumed secondary to increased corticotropin (ACTH) and ACTH-releasing hormone (CRH) secretion. To unmask the proposed increased central (CRH) drive, we administered metyrapone in the AM to 13 depressed and 13 age- and sex-matched normal control subjects. Metyrapone administration resulted in a prompt decrease in plasma cortisol and in an increase in 11-deoxycortisol, the inactive precursor, in all subjects.

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This study examines the extent to which depressive symptoms in female nursing students are affected by specific stressors and coping styles. Three hypotheses were examined for differences in symptoms of depression scores and a model was tested for predicting depression in female nursing students. Responses were gathered from three questionnaires (Hassles and Uplifts Scales, Symptoms of Stress Inventory, and Coping Styles) from 408 female baccalaureate, master's and doctoral students from a major Midwest research university.

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A rate-sensitive fast-feedback inhibition of stress-induced corticotropin secretion by glucocorticoids is well documented in rats. Studies in patients with Cushing's disease or adrenal insufficiency have also supported the existence of fast feedback in humans. However, few studies exist in normal healthy subjects or depressed patients.

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Electroconvulsive therapy is accompanied by an activation of the hypothalamic-pituitary-adrenal axis, resulting in a release of beta-endorphin from the anterior pituitary corticotrophs of humans. As a group, patients in our study demonstrated similar plasma beta-endorphin immunoreactivity response to their initial and final treatments. However, approximately half of the patients demonstrated greater beta-endorphin immunoreactivity release with their first seizure compared with their last seizure, and half of the patients demonstrated the opposite pattern.

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Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, beta-lipotropin-beta-endorphin. We observed a decreased beta-lipotropin-beta-endorphin response in depressed subjects, but a normal adrenal cortisol response.

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Plasma gamma-melanotropin was measured by a gamma 3MSH-specific radioimmunoassay before and after a single bolus intravenous infusion of ovine corticotropin releasing factor (oCRF; 0.1 microgram/kg) in seven normal men. A significant increase of gamma 3MSH was observed 15 minutes post-oCRF infusion, which paralleled a similar increase in plasma cortisol.

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