The Corticosteroid Receptor Hypothesis of Depression

By F. Holsboer. Neuropsychopharmacology, 2000

2,224 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism, Social Psychology

View Paper: https://www.semanticscholar.org/paper/e82e350c4206401e5bc2f41768ec05ba16677f17

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Behavioral Neuroscience

In Endocrinology, Diabetes and Metabolism

In Social Psychology

Citations in the corpus

Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. (2007, background): “Indeed, depressed patients exhibit increased concentrations of CRH in CSF, increased CRH mRNA and protein in the paraventricular nucleus of the hypothalamus (postmortem samples), and a blunted ACTH response to CRH challenge (likely reflecting downregulation of pituitary CRH receptors) (Nemeroff, 199”
The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. (2009, background): “The proper negative feedback via the glucocorticoid receptor thus appears to be critical for a healthy stress response and prolonged or excessive activation of this system have been implicated in the pathogenesis of mood and anxiety disorders (Holsboer, 2000; Pariante and Miller, 2001).”
Stress-Induced p38 Mitogen-Activated Protein Kinase Activation Mediates κ-Opioid-Dependent Dysphoria (2007, background): “…but chronic stress can have adverse effects, including increased risk of depression in humans, increased propensity to participate in drug-seeking behavior, and increased drug-craving in drug-dependent humans and rodents (Holsboer, 2000; McLaughlin et al., 2003a, 2006; Beardsley et al., 2005).”
Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment (2004, neutral): “dtd" [ ]> The stress hormone–regulating hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the causalit”
Current research trends in early life stress and depression: review of human studies on sensitive periods, gene-environment interactions, and epigenetics. (2012, positive): “This fits well with previous hypotheses on the pathogenesis of stressrelated psychiatric disorders, pointing to an important role of HPA axis hyperreactivity (Holsboer, 2000).”
Salivary Cortisol as a Biomarker in Social Science Research (2013, background): “(Holsboer, 2000), while chronic fatigue syndrome is associated with lower overall cortisol levels (Crofford et al.”
The Bargaining Model of Depression (2002, background): “Further, there is evidence that traditional antidepressants may function by effecting changes in corticosteroid receptors, and thus in the HPA axis, changes which then lead to clinical recovery (see Holsboer 2000 and Pariante and Miller 2001 for reviews).”
Household Response to Income Changes: Evidence from an Unconditional Cash Transfer Program in Kenya ∗ (2013, background): “1994) and more permanent stress-related conditions such as major depressive disorder (Holsboer 2000; Hammen 2005).”
THE SHORT-TERM IMPACT OF UNCONDITIONAL CASH TRANSFERS TO THE POOR: EXPERIMENTAL EVIDENCE FROM KENYA (2016, neutral): “…by guest on 25 July 2018 is a useful indicator of both acute stress (Kirschbaum, Strasburger, and Langkrär 1993; Ferracuti et al. 1994) and more permanent stress-related conditions such as major depressive disorder (Holsboer 2000; Hammen 2005).”
Why do we respond so differently? Reviewing determinants of human salivary cortisol responses to challenge. (2009, background): “Further in-depth discussion about underlying mechanisms how such medication impacts on HPA axis stress regulation can be found elsewhere (Barden et al., 1995; Holsboer and Barden, 1996; Holsboer, 2000; Pariante and Miller, 2001).”
The stress system in the human brain in depression and neurodegeneration. (2005, background): “Second, elevated plasma and salivary cortisol and cortisone levels, increased urinary free cortisol excretion, disturbed dexamethasone suppression, decreased corticosteroid receptor function, an enhanced adrenal response to ACTH, a blunted pituitary ACTH response to CRH as well as adrenal and pituit”
Neuroinflammation and depression: A review (2020, background): “…proportion of depressed patients, ranging from 35% to 65%, and are essentially characterized by exaggerated glucocorticoid release and/or increased expression of the adrenocorticotropic hormone (ACTH) secretagogue corticotropin-releasing hormone (Holsboer, 2000; Swaab, Bao, & Lucassen, 2005).”