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Laboratory of Comparative Endocrinology, Zoological Institute, Naamsestraat 61, B-3000 Leuven, Belgium
¹ Laboratory of Hormone Biochemistry, Institute of Biochemistry, Academy of Sciences, Uzbekistan

(Requests for offprints should be addressed to C H J Verhoelst; Email: Carla.Verhoelst{at}bio.kuleuven.ac.be)

It is widely accepted that type II iodothyronine deiodinase (D2) is mostly present in the brain, where it maintains the homeostasis of thyroid hormone (TH) levels. Although intensive studies have been performed on activity and mRNA levels of the deiodinases, very little is known about their expression at the protein level due to the lack of specific antisera. The current study reports the production of a specific D2 polyclonal antiserum and its use in the comparison of D2 protein distribution with that of type I (D1) and type III (D3) deiodinase protein in the choroid plexus at the blood–brain barrier level. Immunocytochemistry showed very high D2 protein expression in the choroid plexus, especially in the epithelial cells, whereas the D1 and D3 proteins were absent. Furthermore, dexamethasone treatment led to an up-regulation of the D2 protein in the choroid plexus. The expression of D2 protein in the choroid plexus led to a novel insight into the working mechanism of the uptake and transport of thyroid hormones along the blood–brain barrier in birds. It is hypothesized that D2 allows the prohormone thyroxine (T₄) to be converted into the active 3,5,3'-triiodothyronine (T₃). Within the choroidal epithelial cells. T₃ is subsequently bound to its carrier protein, transthyretin (TTR), to allow transport through the cerebrospinal fluid. Neurons can thus not only be provided with a sufficient T₃ level via the aid of the astrocytes, as was hypothesized previously based on in situ hybridization data, but also by means of T₄ deiodination by D2, directly at the blood–brain barrier level.

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