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Thyroid Hormone

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Thyroid hormones have been found to be essential for normal neurodevelopment. A deficiency in thyroid hormone (TH) causes hypothyroidism, often due to inadequate levels of iodine. A serious consequence of hypothyroidism during gestation is the development of cretinism in offspring. Cretinism manifests as severe mental retardation, ataxia and sensory deficits, and is the most common preventable cause of brain damage (WHO). Research has shown that even mildly decreased thyroid hormone during this critical period can cause a drop in IQ (Gyamfi, 2009).

Thyroid hormones have significant influence on the development of neurons. TH mediate their effects by binding to thyroid hormone receptors within the cytoplasm that translocate to the nucleus …show more content…
Stimulation of the thyroid gland by Thyroid Stimulating Hormone (TSH) is regulated by a negative feedback mechanism – circulating TH suppresses TSH production. Local levels vary due to different uptake and export mechanisms, interactions with binding proteins in the cytoplasm, and local hormone metabolism. Facilitated transporters are responsible for transporting TH across the blood brain barrier and into the cell, where cytosolic binding proteins regulate TH within the cell. Deiodinases….

Since we saw no differences, could be due to timing:
“The critical time period for thyroid hormone action in rat brain is estimated to extend from around embryonic day 18 (E18) to postnatal day 21–25 (P21–25; Porterfield & Hendrich 1993”.

Another approach would be to look at neuronal cells from different locations in the brain. Perkinje cells in the cerebellum are known to XXXX

Finally, our inconsistent results could be due to preserved stores within the cytosol. The Thyroid-binding protein m crystalline is known to extend the half-life of T4 and help stabilize it. This regulatory protein helps prevent too little or too much TH activating transcription factors within the cell. …show more content…
Delivery of thyroid hormones to the fetal brain is a complex process requiring, at different times, expression of brain thyroid hormone receptors (TRs), materno-fetal thyroid hormone and iodide transport, an intricate system of endocrine feedback (the hypothalamic–pituitary–thyroid (HPT) axis and thyroid hormone metabolism by liver and brain deiodinase enzymes (deiodinase type 2 (D2) and deiodinase type 3 (D3)) to ensure basal levels are sustained ( Zoeller et al. 2007)).

TRs and deiodinase enzymes are expressed in the early brain before the thyroid gland develops ( Obregon et al. 2007). The critical time period for thyroid hormone action in rat brain is estimated to extend from around embryonic day 18 (E18) to postnatal day 21–25 (P21–25; Porterfield & Hendrich 1993). Abnormalities in brain development in hypothyroid rats are mostly seen in the postnatal period and are demonstrated by reduced maturation of key structures such as the cerebellum, where delayed granular cell migration and Purkinje cell maturation are prevented ( Koibuchi et al.

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