Zusammenfassung
Eine Überaktivität des Hypothalamus-Hypophysen-Nebennierenrinden-(HHN-)Systems spielt in der Pathophysiologie der Depression eine Schlüsselrolle. Dies lässt sich besonders gut an Veränderungen des Schlaf-EEGs und der schlafassoziierten Hormonsekretion von Patienten mit Depression zeigen. Gestörter Schlaf, Hyperkortisolismus und verminderte Wachstumshormonausschüttung sind charakteristische neurobiologische Symptome der Depression. Veränderungen im Gleichgewicht der Neuropeptide Corticotropin-freisetzendes Hormon (CRH) und Wachstumshormon-freisetzendes Hormon (GHRH) tragen wesentlich zu diesen Symptomen bei. Während der Hyperkortisolismus und pathologische Ergebnisse neurobiologischer Funktionstests des HHN-Systems als zustandsabhängige Variable bei stabiler Remission sich normalisieren, persistieren Veränderungen von Schlaf-EEG und Wachstumshormon als biologische Narbe langfristig nach Abklingen der psychopathologischen Symptome. Eine Reihe von Daten weist darauf hin, dass eine Normalisierung des HHN-Systems eng mit dem Wirkmechanismus von Antidepressiva verbunden ist. Ein Kronzeuge für diese Hypothese stellt Trimipramin dar. Die logische Konsequenz der Erkenntnisse der neuroendokrinen Grundlagen der Depression ist die Entwicklung von CRH-Antagonisten als neuartiges antidepressives Wirkprinzip.
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Steiger, A. (2002). Neuroendokrinologie der Depression. In: Laux, G. (eds) Depression 2000. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59394-9_3
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