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DHEAS and cortisol correlate with Hypothalamic Serotonin-1A Receptors
Annals of General Psychiatry volume 7, Article number: S220 (2008)
Serotonin modulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis, to a big part through the serotonin-1A receptor (5-HT1A) . In return, hormones of the HPA axis, namely dehydroepiandrosterone sulfate (DHEAS)  and cortisol have regulatory effects on the serotonergic neurotransmission.
Materials and methods
Eighteen healthy female subjects participated in this PET study. The selective 5-HT1A receptor antagonist [carbonyl-11C]WAY-100635 was used as radioligand. The hypothalamus as an essential part of the HPA axis and eight control regions of interest and the cerebellum as reference region were defined a priori and delineated on co-registered MR images. DHEAS and cortisol plasma levels were ascertained by morning blood collections on the PET day. The 5-HT1A receptor binding potentials of the target brain regions were correlated with DHEAS, cortisol plasma levels and the ratio of DHEAS / cortisol.
We found highly significant correlations between the hypothalamic 5-HT1A receptor binding and DHEAS (p=.003) and the ratio of DHEAS / cortisol (p<.0001), but not with cortisol and not in other brain regions.
The 5-HT1A receptor may influence the DHEAS plasma level by modulating CRH and ACTH release as reported for cortisol before . Vice versa, the interaction of cortisol and DHEAS may exert a regulatory effect on the 5-HT1A receptor distribution in the hypothalamus as a feedback loop. As disturbances of the HPA axis  as well as changes of the 5-HT1A receptor distribution  have been reported frequently in affective disorders, future studies should aim their focus on these interactions.
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This research was supported by grants from the Austrian National Bank (OENB P11468) and the Medical Science Fund of the City of Vienna (BMF P2515) to R. Lanzenberger, and a grant from the Austrian Science Fund (FWF P16549). The authors are grateful to J. Tauscher, C. Windischberger, A. Becherer, N. Praschak-Rieder, L. Pezawas, M. Willeit, M. Fink, D. Ettlinger, T. Attarbaschi, S. Friedreich, E. Moser, and R. Dudczak for their scientific, medical or administrative support.