Tanycytes control the hormonal output of the hypothalamic-pituitary-thyroid axis

Helge Müller-Fielitz (), Marcus Stahr, Mareike Bernau, Marius Richter, Sebastian Abele, Victor Krajka, Anika Benzin, Jan Wenzel, Kathrin Kalies, Jens Mittag, Heike Heuer, Stefan Offermanns and Markus Schwaninger ()
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Helge Müller-Fielitz: University of Lübeck
Marcus Stahr: University of Lübeck
Mareike Bernau: University of Lübeck
Marius Richter: University of Lübeck
Sebastian Abele: University of Lübeck
Victor Krajka: University of Lübeck
Anika Benzin: University of Lübeck
Jan Wenzel: University of Lübeck
Kathrin Kalies: University of Lübeck
Jens Mittag: University of Lübeck
Heike Heuer: Leibniz Research Institute for Environmental Medicine
Stefan Offermanns: Max-Planck-Institute for Heart and Lung Research
Markus Schwaninger: University of Lübeck

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract The hypothalamic–pituitary–thyroid (HPT) axis maintains circulating thyroid hormone levels in a narrow physiological range. As axons containing thyrotropin-releasing hormone (TRH) terminate on hypothalamic tanycytes, these specialized glial cells have been suggested to influence the activity of the HPT axis, but their exact role remained enigmatic. Here, we demonstrate that stimulation of the TRH receptor 1 increases intracellular calcium in tanycytes of the median eminence via Gαq/11 proteins. Activation of Gαq/11 pathways increases the size of tanycyte endfeet that shield pituitary vessels and induces the activity of the TRH-degrading ectoenzyme. Both mechanisms may limit the TRH release to the pituitary. Indeed, blocking TRH signaling in tanycytes by deleting Gαq/11 proteins in vivo enhances the response of the HPT axis to the chemogenetic activation of TRH neurons. In conclusion, we identify new TRH- and Gαq/11-dependent mechanisms in the median eminence by which tanycytes control the activity of the HPT axis.

Date: 2017
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DOI: 10.1038/s41467-017-00604-6

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