作者: Pierre J. Neveu , Nathalie Castanon
DOI: 10.1007/978-0-585-37970-8_15
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摘要: Depression is a complex disease which likely to involve several pathophysiological pathways. There clear evidence that depression associated with neurochemical and neuroendocrine alterations. Reduced activity of the serotoninergic (5-HT) noradrenergic (NA) central systems are observed in majority patients major (Garver & Davis, 1979). Depressed usually also exhibit an alteration hypothalamus-pituitary-adrenal (HPA) axis characterized by hyperproduction corticotropin-releasing hormone (CRH), stimulates adrenocorticotropic (ACTH) cortisol release (Holsboer, Bardeleben, Gerken, Stalla, Muller, 1984). Therefore, biochemical most antidepressants, including selective 5-HT reuptake inhibitors, monoamine oxidase tricyclic has been assessed on basis their ability reverse alterations and/or HPA activities (Hollister, 1986). However, metabolic these drugs not necessarily related directly clinical efficacy (Barden, Reul, Holsboer, 1995; Blier de Montigny, 1994). Despite repeated attempts, neuro-hormonal abnormalities have never shown predict therapeutic response, nor can they account for symptomatic profile patients. Furthermore, depletion or NA healthy individuals does induce clinically significant depressive symptomatology (Young, Smith, Pihl, Erwin, 1985). In addition, there some atypical antidepressants known experimental effects, but devoid classic antidepressant actions (Guelfi, 1992; Van Riezen Leonard, 1990).