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Glucocorticoids and the Genesis of Depressive Illness a Psychobiological Model
Ist Teil von
British journal of psychiatry, 1994-03, Vol.164 (3), p.365-371
Ort / Verlag
Cambridge, UK: Cambridge University Press
Erscheinungsjahr
1994
Link zum Volltext
Quelle
Applied Social Sciences Index & Abstracts (ASSIA)
Beschreibungen/Notizen
Abnormalities in the hypothalamic–pituitary–adrenal axis (HPA) have been the most consistently demonstrated biological markers in depressive illness. Numerous other neuroendocrine disturbances have also been described, including blunted clonidine-induced growth hormone release and blunted fenfluramine-induced prolactin release. These disturbances are generally interpreted in terms of monoaminergic receptor dysfunction. The theory presented here suggests that chronic stress which activates the HPA will in certain susceptible people produce changes in central monoamines. The high level of glucocorticoid receptors on such central neurons is postulated as mediating the alterations. Thus monoamine abnormalities, rather than being a core aetiological feature of depression, are seen as secondary to HPA overdrive.