Cortisol response to intramuscular desipramine in patients with major depression and normal control subjects: A replication study
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Effects of escitalopram/quetiapine combination therapy versus escitalopram monotherapy on hypothalamic-pituitary-adrenal-axis activity in relation to antidepressant effectiveness
2014, Journal of Psychiatric ResearchCitation Excerpt :Furthermore, depressive symptoms were also reduced under ESC monotherapy, which was not accompanied by significant HPA axis modulation. It has previously been suggested that several antidepressants such as reboxetine, SSRIs or tricyclic antidepressants acutely stimulate cortisol secretion in healthy subjects (Schule, 2007) as well as in depressive patients (Asnis et al., 1992). These compounds may slowly normalize HPA system hyperactivity when administered for several weeks via up-regulation of mineralocorticoid receptor and glucocorticoid receptor mRNA (Brady et al., 1991; Seckl and Fink, 1992) and decrease of CRH gene expression and CRH mRNA synthesis in the paraventricular nucleus (Mori et al., 1998; Stout et al., 2002).
Impact on cortisol and antidepressant efficacy of quetiapine and escitalopram in depression
2014, PsychoneuroendocrinologyCitation Excerpt :This study supports the general assumption, that a long-term normalization of the HPA axis hyperactivity is a correlate of clinical improvement (response), regardless of the mechanism of action of the antidepressant drug and regardless of the initial changes of the HPA axis during week 1. Regarding the underlying mechanisms, it can by hypothesized that reuptake inhibiting antidepressants such as reboxetine, SSRIs or tricyclic antidepressants acutely stimulate COR secretion both in healthy subjects (Laakmann, 1988; Schule, 2007) and in depressed patients (Asnis et al., 1992) after single administration and may gradually normalize HPA axis hyperactivity in depressed patients when administered daily for several weeks via up-regulation of mineralocorticoid receptor and glucocorticoid receptor mRNA levels (Brady et al., 1991; Seckl and Fink, 1992), down-regulation of pro-opiomelanocortin mRNA expression in the pituitary gland (Jensen et al., 2001), and decrease of CRH gene expression and CRH mRNA synthesis in the paraventricular nucleus (Mori et al., 1998; Stout et al., 2002), thereby enhancing mineralocorticoid receptor and glucocorticoid receptor function and restoring the disturbed feedback control (“reset” mechanism). It can also be assumed that these effects of antidepressants on gene expression represent physiological adaptive mechanisms which are triggered by the primarily acute stimulatory effects of reuptake inhibitors on the ACTH and COR release and take several weeks to become effective.
Influence of mirtazapine on urinary free cortisol excretion in depressed patients
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