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Submitted on September 3, 2004
Accepted on January 11, 2005
Max Planck Institute for Experimental Endocrinology, D-30625 Hannover, Germany; Institute of Molecular Biotechnology, D-07745 Jena, Germany; Department of Internal Medicine, Erasmus MC, 3015 GE Rotterdam, The Netherlands
* To whom correspondence should be addressed. E-mail: hheuer{at}imb-jena.de.
Recent genetic analysis in several patients presenting a severe form of X-linked psychomotor retardation combined with abnormal thyroid hormone (TH) levels have revealed mutations or deletions in the gene of the monocarboxylate transporter 8 (MCT8). Since in vitro MCT8 functions as a TH transporter, the complex clinical picture of these patients indicated an important role of MCT8 in TH-dependent processes of brain development. To provide a clue as to the cellular function of MCT8 in brain, we studied the expression of MCT8 mRNA in the murine CNS by in situ hybridization histochemistry (ISH). In addition to the choroid plexus structures, highest transcript levels were found in neo- and allocortical regions (e.g. in the olfactory bulb, cerebral cortex, hippocampus and amygdala), moderate signal intensities in the striatum and the cerebellum and low levels in a few neuroendocrine nuclei. Colocalization studies revealed that MCT8 is predominantly expressed in neurons. Together with the spatiotemporal expression pattern of MCT8 during perinatal life periods, these results strongly indicate that MCT8 plays an important role for proper CNS development by transporting TH into neurons as its main target cells.
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