No abstract

The effect of estradiol and thyroid hormone treatment on pituitary TRH binding and TSH and PRL responses to the neurohormone was studied. A significant increase in the number of pituitary TRH binding sites was observed between 2 and 4 days after daily administration of estradiol benzoate with a plateau at 300% of control being reached at 7 days. Plasma PRL levels showed a similar early pattern of response. In animals rendered hypothyroid by a 2-month treatment with propylthiouracil or 1 month after surgical thyroidectomy, the level of pituitary TRH receptors was increased approximately 2-fold, this elevation being completely reversed by treatment with thyroid hormone. Estradiol-17beta administered with L-thyroxine partially reversed the inhibitory effect of thyroid hormone on TRH receptor levels in hypothyroid animals. The antagonism between estrogens and thyroid hormone is also apparent on the TSH response to TRH since estrogen administration can reverse the marked inhibition by thyroxine of the TSH response to TRH either partially or completely in intact and hypothyroid animals, respectively. The PRL response to TRH is 55 and 40% inhibited in hypothyroid and intact rats, respectively, by thyroid hormone when combined with estrogen treatment. The present data clearly show that estrogens and thyroid hormones can affect TSH and PRL secretion, the effect of estrogens being predominantly on PRL secretion while thyroid hormone affects mainly TSH. The close correlation observed between the level of TRH receptors and PRL and TSH responses to TRH suggests that estrogens and, to a lesser extent, thyroid hormones, exert their action by modulation of the level of receptors for the neurohormone in both thyrotrophs and mammotrophs.

No significant change in hypothalamic TRH content was found in rats during acute (5–240 min) exposure to cold (5 °C), in spite of rapid and sustained elevations in plasma TSH and thyroxine. Plasma PRL rose markedly in the first 15 min, but returned to normal thereafter. Chronic exposure to cold (32 days) was characterized by elevated plasma and pituitary levels of both TSH and PRL in the presence of an unaltered hypothalamic TRH content. If increased TRH release from the hypothalamus occurs during exposure to cold, as suggested by the pituitary-thyroid stimulation, either it is compensated for by an equal rise in synthesis, or the extra amount released is negligible in comparison with the hypothalamic content of TRH. The acute PRL response to exposure to cold may be related to an acute TRH release but could also result from the accompanying stress response acting by a mechanism independent of TRH.