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Congenital Hypothyroidism (Cretinism) in neuroD2-Deficient Mice

Clinical Research,¹ Human Biology Divisions, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, and Departments of,² Neurology,³ Pathology,⁴ Pediatrics and Programs in,⁵ Neurobiology and Behavior,⁶ Molecular and Cellular Biology, University of Washington, Seattle, Washington 98105⁷

Received 7 November 2005/ Returned for modification 9 December 2005/ Accepted 9 March 2006

Mice lacking neuroD2, a basic helix-loop-helix transcription factor involved in brain development, show growth retardation and other abnormalities consistent with hypothalamic-pituitary-thyroid (HPT) axis dysfunction. neuroD2 is expressed in the paraventricular hypothalamic nuclei, the anterior lobe of pituitary, and the thyroid gland. In neuroD2-deficient mice, thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormone are decreased in these three regions, respectively. neuroD2-null mice typically die 2 to 3 weeks after birth, but those treated with replacement doses of thyroxine survived more than 8 weeks. These data indicate that neuroD2 is expressed throughout the HPT axis and that all levels of the axis are functionally affected by its absence in mice.