Seasonality-resilient individuals downregulate their cerebral 5-HT transporter binding in winter – A longitudinal combined 11C-DASB and 11C-SB207145 PET study.

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Seasonality-resilient individuals downregulate their cerebral 5-HT transporter binding in winter – A longitudinal combined 11C-DASB and 11C-SB207145 PET study.

Eur Neuropsychopharmacol. 2018 Aug 01;:

Authors: Mc Mahon B, Nørgaard M, Svarer C, Andersen SB, Madsen MK, Baaré WFC, Madsen J, Frokjaer VG, Knudsen GM

Abstract
We have recently shown that the emergence and severity of seasonal affective disorder (SAD) symptoms in the winter is associated with an increase in cerebral serotonin (5-HT) transporter (SERT) binding. Intriguingly, we also found that individuals resilient to SAD downregulate their cerebral SERT binding in the winter. In the present paper, we provide an analysis of the SERT- and 5-HT dynamics as indexed by 5-HT4 receptor (5-HT4R) binding related to successful stress coping. We included 46 11C-DASB positron emission tomography (PET) scans (N = 23, 13 women, age: 26 ± 6 years) and 14 11C-SB207145 PET scans (7 participants, 3 women, age: 25 ± 3 years) from 23 SAD-resilient Danes. Data was collected longitudinally in summer and winter. We found that compared to the summer, raphe nuclei and global brain SERT binding decreased significantly in the winter (praphe = 0.003 and pglobal = 0.003) and the two measures were positively correlated across seasons (summer: R2 = 0.33, p = .004, winter: R2 = 0.24, p = .018). A voxel-based analysis revealed prominent changes in SERT in clusters covering both angular gyri (0.0005 < pcorrected < 0.0016), prefrontal cortices (0.00087 < pcorrected < 0.0039) and the posterior temporal and adjacent occipital cortices (0.0001 < pcorrected < 0.0066). We did not observe changes in 5-HT4R binding, suggesting that 5-HT levels remained stable across seasons. We conclude that resilience to SAD is associated with a global downregulation of SERT levels in winter which serves to keep 5-HT levels across seasons.

PMID: 30077433 [PubMed – as supplied by publisher]

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Paroxetine blunts the corticosterone response to swim-induced stress and increases depressive-like behavior in a rat model of postpartum depression.

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Paroxetine blunts the corticosterone response to swim-induced stress and increases depressive-like behavior in a rat model of postpartum depression.

Psychoneuroendocrinology. 2017 Oct 31;:

Authors: Overgaard A, Lieblich SE, Richardson R, Galea LAM, Frokjaer VG

Abstract
Perinatal depression (PND) affects 15% of women. During the perinatal period both stress- and gonadal hormones fluctuate widely. Putatively, these fluctuations are involved in PND disease mechanisms. The serotonin system is sensitive to such hormone fluctuations, and serotonin reuptake inhibitors (SSRIs) are used to treat PND, although treatment is suboptimal and it is not known at which peripartum time-point SSRI treatment may be most efficacious. In this study, we investigate the effect of the SSRI paroxetine (5mg/kgs.c.) on swim stress-induced corticosterone in a rat model of postpartum depression. In the rat model corticosterone (CORT; 40mg/kgs.c.) was administered in Sprague Dawley rats across postpartum day (PD)2 to PD14. Stress response was measured during the first exposure to the forced swim test (FST1), and depressive-like behavior was measured in both FST1 and FST2. We found that paroxetine completely blunted the swim stress-induced CORT response and increased depressive-like behavior in both FST1 and FST2. Our findings suggest that in the postpartum context, SSRIs compromise stress axis dynamics, which are needed for a healthy stress response. This is likely unfavorable for reversing depressive-like behavior and may provide a rationale for augmentation strategies beyond SSRIs alone to optimize the clinical management of PND.

PMID: 29146408 [PubMed – as supplied by publisher]

Source: My publications feed from NCBI