Abstract
This study was designed to determine the effect of neonatally-produced hypothyroidism on reserpine-elicited tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DβH) induction in the superior cervical ganglion (SCG) in rats. Some rats were rendered hypothyroid from birth by daily treatment with propylthiouracil (PTU). Some hypothyroid rats received replacement therapy with triiodothyronine (T 3). Some rats received PTU for 20 days, beginning at 90 days of age. Some rats were not treated and served as controls. TH and DβH activities were assayed at 30, 50 and 110 days of age. Basal TH activity in the SCG for rats made hypothyroid as neonates was significantly lower than for controls at all ages tested; basal DβH activity for these rats was lower than for controls at 30 and 50 days of age, but by 110 days was not different from that for controls. Basal TH activity for rats made hypothyroid as adults was intermediate between that for controls and rats made hypothyroid from infancy. Injecting control rats with reserpine produces a robust TH induction in the SCG at each age tested, and a strong DβH induction at 50 and 110 days of age. Reserpine-evoked TH and DβH inductions in rats made hypothyroid as adults were not different from those seen in controls. In contrast, rats made hypothyroid from infancy showed virtually no evidence of a reserpine-provoked TH or DβH induction at any age tested. TH and DβH inductions for hypothyroid rats given T 3 replacement were completely normal. Thus, although the presence of thyroid hormones per se is not required for either TH or DβH induction in the SCG, thyroid hormones acting during infancy seem to be important for the development of the capacity for TH and DβH induction in this tissue.
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