AENDO November 40/5

Yuan, Pu-Qing, and Hong Yang. Hypothyroidism induces Fos-like immunoreactivity in ventral medullary neurons that synthesize TRH. Am. J. Physiol. 277 (Endocrinol. Metab. 40): E927–E936, 1999.—Altered thyroid statuses are associated with autonomic disorders. Thyrotropin-releasing hormone (TRH) in medullary nuclei regulates vagal efferent activity. Induction of Fos-like immunoreactivity (IR) in medullary TRH-synthesizing neurons was investigated in 24-h fasted rats with different thyroid statuses. Hypoand hyperthyroidism were induced by 6-N-propyl-2-thiouracil (PTU) in drinking water and a daily intraperitoneal injection of thyroxine (T4; 10 μg·100 g21 ·day21), respectively, for 1–4 wk. The numbers of Fos-like IR positive neurons in the raphe pallidus, raphe obscurus, and parapyramidal regions, which were low in euthyroid rats (0–2/section), increased remarkably as the hypothyroidism progressed and were negatively correlated with serum T4 levels. At the 4th wk, Fos-like IR positive neurons were 10to 70-fold higher compared with euthyroid controls. Simultaneous T4 replacement (2 μg·100 g21 ·day21) prevented the increases of Fos-like IR in PTU-treated rats. Hyperthyroidism did not change the number of Fos-like IR neurons in the raphe nuclei but reduced it in the parapyramidal regions. Double immunostaining revealed that most of the Fos-like IR induced by hypothyroidism was located in the prepro-TRH IR positive neurons. The selective and sustained induction of Fos-like IR in TRH-synthesizing neurons in ventral medullary nuclei by hypothyroidism indicates that these neurons play a role in the autonomic disorders observed in altered thyroid statuses.