Exogenous Triiodothyronine Lowers Thyrotropin-Releasing Hormone Concentrations in the Specific Hypothalamic Nucleus (Paraventricular) Involved in Thyrotropin Regulation and also in Posterior Nucleus

Recent evidence indicates that thyroid hormones can regulate thyrotropin secretion in vivo in part by inhibiting thyrotropin-releasing hormone (TRH) secretion itself. Therefore, to explore whether triiodothyronine (T<sub>3</sub>) interacts with the specific hypothalamic area involved in thyrotropin (TSH) secretory regulation, the paraventricular nucleus (PVN), Palkovitz micropunches from eight nuclear regions were obtained from 1,000-µm frozen coronal brain slices for immunoassay determinations of TRH. Rats were treated either with parenteral L-T3 for 6 days to induce experimental thyrotoxicosis, or 0.15 M saline. The induction of thyrotoxicosis was confirmed by demonstrating that mean plasma TSH concentrations fell from 108 to < 10 µU/ml (p < 0.01). TRH concentrations in the PVN were reduced concomitantly after L-T<sub>3</sub> from 1.9 to 1.1 ng/mg protein (p < 0.05). No reductions in TRH concentrations during T<sub>3</sub> treatment occurred in other nuclear groupings except in the posterior hypothalamic nucleus. Total TRH content in the median eminence declined also in T<sub>3</sub>-treated animals from 1.77 to 1.29 ng, representing a 32% reduction (p < 0.01). No signifcant change was seen in the median eminence content of the TRH structurally related dipeptide, cyclo(His-Pro). The data herein indicate that experimental thyrotoxicosis in the rat is associated with a selective reduction in TRH concentrations in the PVN, documenting T3 effects upon hypothalamic TRH metabolism per se.