Cellular thyroid hormone uptake and efflux are mediated by transmembrane 
transport proteins. One of these, monocarboxylate transporter 8 (MCT8) is 
mutated in Allan-Herndon-Dudley syndrome, a severe mental retardation associated 
with abnormal thyroid hormone constellations. Since mice deficient in Mct8 
exhibit a milder neurological phenotype than patients, we hypothesized that 
alternative thyroid hormone transporters may compensate in murine brain cells 
for the lack of Mct8. Using qPCR, Western Blot, and immunocytochemistry, we 
investigated the expression of three different thyroid hormone transporters, 
i.e., Mct8 and L-type amino acid transporters Lat1 and Lat2, in mouse brain. All 
three thyroid hormone transporters are expressed from corticogenesis and peak 
around birth. Primary cultures of neurons and astrocytes express Mct8, Lat1, and 
Lat2. Microglia specifically expresses Mct10 and Slco4a1 in addition to high 
levels of Lat2 mRNA and protein. As in vivo, a brain microvascular endothelial 
cell line expressed Mct8 and Lat1. 158N, an oligodendroglial cell line expressed 
Mct8 protein, consistent with delayed myelination in MCT8-deficient patients. 
Functional T(3)- and T(4)-transport assays into primary astrocytes showed K(M) 
values of 4.2 and 3.7 μM for T(3) and T(4). Pharmacological inhibition of L-type 
amino acid transporters by BCH and genetic inactivation of Lat2 reduced 
astrocytic T(3) uptake to the same extent. BSP, a broad spectrum inhibitor, 
including Mct8, reduced T(3) uptake further suggesting the cooperative activity 
of several T(3) transporters in astrocytes.