Anatomy of melancholia: focus on hypothalamic-pituitary-adrenal axis overactivity and the role of vasopressin.
Dinan, Timothy G Scott, Lucinda V
Dinan, Timothy G
Scott, Lucinda V
Author
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Date
2012-02-03T15:06:29Z
Date Submitted
Keywords
Other Subjects
Subject Mesh
Adrenocorticotropic Hormone/physiology
Depressive Disorder/*physiopathology
Feedback, Physiological
Glucocorticoids/physiology
Humans
Hydrocortisone/physiology
Hypothalamo-Hypophyseal System/*physiology
Neurons/metabolism
Pituitary-Adrenal System/*physiology
Receptors, Vasopressin/metabolism
Stress, Psychological
Vasopressins/*physiology
Depressive Disorder/*physiopathology
Feedback, Physiological
Glucocorticoids/physiology
Humans
Hydrocortisone/physiology
Hypothalamo-Hypophyseal System/*physiology
Neurons/metabolism
Pituitary-Adrenal System/*physiology
Receptors, Vasopressin/metabolism
Stress, Psychological
Vasopressins/*physiology
Planned Date
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Abstract
Overactivity of the hypothalamic-pituitary-adrenal (HPA) axis characterized by hypercortisolism, adrenal hyperplasia and abnormalities in negative feedback is the most consistently described biological abnormality in melancholic depression. Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are the main secretagogues of the HPA/stress system. Produced in the parvicellular division of the hypothalamic paraventricular nucleus the release of these peptides is influenced by inputs from monoaminergic neurones. In depression, anterior pituitary CRH1 receptors are down-regulated and response to CRH infusion is blunted. By contrast, vasopressin V3 receptors on the anterior pituitary show enhanced response to AVP stimulation and this enhancement plays a key role in maintaining HPA overactivity.
Language
eng
Citation
ISSN
0021-8782 (Print)
0021-8782 (Linking)
0021-8782 (Linking)
eISSN
ISBN
DOI
10.1111/j.1469-7580.2005.00443.x
PMID
16185250