Repeated citalopram treatment but not stress exposure attenuates hypothalamic-pituitary-adrenocortical axis response to acute citalopram injection

Moncek, Fedor; Dunčko, Roman; Ježová, Daniela

doi:10.1016/s0024-3205(02)02409-8

Cited by 20 publications

(11 citation statements)

References 44 publications

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“…Moncek et al (2003) showed that after repeated administration of R/S-CIT, ACTH release was attenuated as compared to that after a single dose. Plasma corticosterone levels also rose during repeated R/S-CIT treatment, but there were no differences compared to a single dose within the time interval studied.…”

Section: Discussionmentioning

confidence: 97%

“…Studies in the rat have suggested that acute R/S-CIT administration activated the HPA axis at the hypothalamic level and long-term R/S-CIT treatment desensitized the HPA axis at the pituitary level (Jensen et al 1999;Moncek et al 2003). Moncek et al (2003) showed that after repeated administration of R/S-CIT, ACTH release was attenuated as compared to that after a single dose.…”

Section: Discussionmentioning

confidence: 99%

“…Such suppressive effect on HPA axis activity was demonstrated in rats under both basal and stress conditions for a number of antidepressant drugs, e.g., R/S-CIT (Jensen et al 1999;Moncek et al 2003). Since therapeutic effects of antidepressants are seen first after 2-3 weeks of treatment, it is a plausible assumption that long-term adaptive changes are important for their mechanism of action.…”

Section: Introductionmentioning

confidence: 98%

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Long-term citalopram administration reduces responsiveness of HPA axis in patients with major depression: relationship with S-citalopram concentrations in plasma and cerebrospinal fluid (CSF) and clinical response

et al. 2005

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Rationale: A dysregulation of the hypothalamicpituitary-adrenal (HPA) axis is a well-documented neurobiological finding in major depression. Moreover, clinically effective therapy with antidepressant drugs may normalize the HPA axis activity. Objective: The aim of this study was to test whether citalopram (R/S-CIT) affects the function of the HPA axis in patients with major depression (DSM IV). Methods: Twenty depressed patients (11 women and 9 men) were challenged with a combined dexamethasone (DEX) suppression and corticotropin-releasing hormone (CRH) stimulation test (DEX/CRH test) following a placebo week and after 2, 4, and 16 weeks of 40 mg/day R/S-CIT treatment. Results: The results show a time-dependent reduction of adrenocorticotrophic hormone (ACTH) and cortisol response during the DEX/CRH test both in treatment responders and nonresponders within 16 weeks. There was a significant relationship between post-DEX baseline cortisol levels (measured before administration of CRH) and severity of depression at pretreatment baseline. Multiple linear regression analyses were performed to identify the impact of psychopathology and hormonal stress responsiveness and R/S-CIT concentrations in plasma and cerebrospinal fluid (CSF). The magnitude of decrease in cortisol responsivity from pretreatment baseline to week 4 on drug [delta-area under the curve (AUC) cortisol] was a significant predictor (p<0.0001) of the degree of symptom improvement following 16 weeks on drug (i.e., decrease in HAM-D 21 total score). The model demonstrated that the interaction of CSF S-CIT concentrations and clinical improvement was the most powerful predictor of AUC cortisol responsiveness. Conclusion: The present study shows that decreased AUC cortisol was highly associated with S-CIT concentrations in plasma and CSF. Therefore, our data suggest that the CSF or plasma S-CIT concentrations rather than the R/S-CIT dose should be considered as an indicator of the selective serotonergic reuptake inhibitors (SSRIs) effect on HPA axis responsiveness as measured by AUC cortisol response.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Long-term citalopram administration reduces responsiveness of HPA axis in patients with major depression: relationship with S-citalopram concentrations in plasma and cerebrospinal fluid (CSF) and clinical response

et al. 2005

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“…Unfortunately, these data have never been reconciled with our understanding that elevation of serotonin increases stress resilience. A recent study showed that repeated citalopram treatment decreased CRH and HPA axis activity in rodents, raising the possibility that discrepancies may be due to chronic versus acute treatments with serotonergic ligands (Moncek et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Ovarian Steroid Treatment Decreases Corticotropin-Releasing Hormone (CRH) mRNA and Protein in the Hypothalamic Paraventricular Nucleus of Ovariectomized Monkeys

Bethea

Centeno

2007

Neuropsychopharmacol

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Corticotropin-releasing hormone (CRH) gene and protein expression were examined in the paraventricular nucleus (PVN) of ovariectomized female macaques treated with placebo or hormone therapy (HT) consisting of either estrogen (E) for 28 days, or progesterone (P) for the last 14 of 28 days, or E for 28 days supplemented with P for the last 14 of 28 days using Silastic capsules implanted s.c. in the periscapular region (n ¼ 4/group). Perfusion fixed sections (25 mm) at five levels of the PVN (rostral to caudal at 250 mm intervals) were immunostained (ICC) with an antibody to human CRH or processed in an in situ hybridization (ISH) assay with a monkey specific CRH riboprobe. The immunostained CRH-positive area was quantified with a Marianas Stereology Workstation and Slidebook 4.2. There was a significant decrease in the immunological CRH signal with E, P, and E + P treatment as measured by total or average pixels and microns (analysis of variance (ANOVA), po0.002; Student-Newman-Keul's post hoc test versus placebo control group, po0.05). There was also a decrease in the number of detectable CRH neurons (ANOVA, po0.03) with HT. The sections processed for ISH were exposed to autoradiographic films. The CRH mRNA signal was analyzed with NIH Image. The average optical density and positive pixel area of the CRH mRNA signal was significantly suppressed by ovarian HT (ANOVA po0.002; StudentNewman-Keul's post hoc test versus placebo control group, po0.05). In summary, 1 month of stable treatment with a moderate dose of E, P or E + P significantly reduced CRH mRNA and protein in the PVN of ovariectomized monkeys. These results suggest that this hormone treatment regimen may increase stress resilience in surgically menopausal primates.

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“…[86][87][88][89] A slight rise in CRH may be detected immediately after starting treatment with citalopram, which turns into a decrease after continuous administration. 90 We have demonstrated that leptin replacement therapy in leptin-deficient adults with established pathological obesity results not only in profound weight loss and behavioral effects, but also in changes on the endocrine stress axis. 91 These findings show that both antiobesity and antidepressive medication decrease the activation of the HPA axis to a great extent, leading to a reduction in ACTH and cortisol.…”

Section: A B C D E F G Hmentioning

confidence: 99%

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

et al. 2006

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Obesity and depression are serious public health problems and also constitute cardiovascular disease risk factors. Research organizations have called for efforts to explore the interrelationship between obesity and depression. A useful starting point is the fact that in both disorders there is dysregulation of stress systems. We review molecular and clinical evidence indicating that the mediators of the stress response are a key locus for geneenvironment interactions in the shared biology of depression and obesity. Scientific milestones include translational paradigms such as mice knockouts, imaging and pharmacogenomic approaches that can identify new therapeutic strategies for those burdened by these two afflictions of contemporary civilization. Perspectives for the future are promising. Our ability to dissect the underpinnings of common and complex diseases with shared substrates will be greatly enhanced by the Genes and Environment Initiative, the emerging Large Scale Studies of Genes and Environment in Common Disease, and the UK Biobank Project.

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Repeated citalopram treatment but not stress exposure attenuates hypothalamic-pituitary-adrenocortical axis response to acute citalopram injection

Cited by 20 publications

References 44 publications

Long-term citalopram administration reduces responsiveness of HPA axis in patients with major depression: relationship with S-citalopram concentrations in plasma and cerebrospinal fluid (CSF) and clinical response

Long-term citalopram administration reduces responsiveness of HPA axis in patients with major depression: relationship with S-citalopram concentrations in plasma and cerebrospinal fluid (CSF) and clinical response

Ovarian Steroid Treatment Decreases Corticotropin-Releasing Hormone (CRH) mRNA and Protein in the Hypothalamic Paraventricular Nucleus of Ovariectomized Monkeys

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

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