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Submitted on December 22, 2006
Accepted on February 13, 2007
Departments of Physiology and Medicine, Dartmouth Medical School, 1 Medical Center Drive, Lebanon, NH 03756. Department of Psychology and Brain Sciences, Dartmouth College, Hanover, NH 03755
* To whom correspondence should be addressed. E-mail: Val.galton{at}dartmouth.edu.
Considerable indirect evidence suggests that the type 2 deiodinase (D2) generates 3,5,3'-triodothyronine (T3) from thyroxine (T4) for "local" use in specific tissues such and pituitary, brown fat (BAT) and brain, and studies with a D2-deficent mouse (D2KO) have shown this to be the case in pituitary and BAT. The present study employs the D2KO to determine the role of D2 in the developing brain. As expected, the T3 content in the neonatal D2KO brain was markedly reduced to a level comparable to that seen in the hypothyroid neonatal WT mouse. However, the mRNA levels of several T3-responsive genes were either unaffected or much less affected in the brain of the D2KO mouse than in that of the hypothyroid mouse, and compared with the hypothyroid mouse, the D2KO mouse exhibited a very mild neurological phenotype. The current view of thyroid hormone homeostasis in the brain dictates that the T3 present in neurons is generated mostly, if not exclusively from T4 by the D2 in glial cells. This view is inadequate to explain the findings presented herein, and it is suggested that important compensatory mechanisms must be in play in the brain to minimize functional abnormalities in the absence of the D2.
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