Anatomy of melancholia: focus on hypothalamic-pituitary-adrenal axis overactivity and the role of vasopressin.
Affiliation
Department of Psychiatry and Alimentary Pharmabiotic Centre, Cork University, Hospital, Ireland. t.dinan@ucc.ieIssue Date
2012-02-03T15:06:29ZMeSH
Adrenocorticotropic Hormone/physiologyDepressive 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
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J Anat. 2005 Sep;207(3):259-64.Journal
Journal of anatomyDOI
10.1111/j.1469-7580.2005.00443.xPubMed ID
16185250Abstract
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
engISSN
0021-8782 (Print)0021-8782 (Linking)
ae974a485f413a2113503eed53cd6c53
10.1111/j.1469-7580.2005.00443.x
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