Corticotropin-Releasing Factor in Depression and Suicide
Hypothalamic-pituitary-adrenocortical (HPA) axis hyperactivity is one of the most consistent findings in major depression (Carroll 1982; Halbreich et al. 1985; Carroll 1985). However, the regulation of HPA activity in humans is highly complex, and the mechanism of Cortisol overproduction together with impaired suppressibility by exogenous steroids is far from being understood. One possibility is a primary overproduction of the principal adrenocorticotropic hormone (ACTH)-stimulating hypothalamic substance: corticotropin-releasing factor (CRF), a 41-amino acid peptide isolated and characterized by Vale et al. (1981). At present there are two lines of evidence favoring this hypothesis: first, Gold et al. (1984) showed that depressed patients responded with a lower ACTH rise to intravenously administered CRF than nondepressed patients or healthy controls, consistent with a down regulation of the pituitary CRF receptors. Second, our group reported that in psychiatric patient groups from different countries (including the USA, Sweden, and Hungary) there was a fairly specific increase in lumbar CSF CRF concentration in subjects with major unipolar and bipolar depression compared with other diagnostic groups (schizophrenia, senile dementia, anxiety disorders, etc.) or with healthy controls (Nemeroff et al. 1984; Bissette et al. 1985).
KeywordsDepression Lithium Dementia Cortisol Schizophrenia
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