Effect of Chronic Immunoneutralization of Thyrotropin-Releasing Hormone on the Hypothalamic-Pituitary-Thyroid Axis, Prolactin, and Reproductive Function in the Ewe

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Abstract
The physiological role of TRH was studied by chronic neutralization of its action by actively immunizing six adult ewes against the synthetic TRH conjugated to BSA. The animals were followed for a period of 2 yr through the various reproductive states of estrous cyclicity, anestrus, pregnancy, and lactation and were subjected to tests known to stimulate PRL release. Changes in plasma concentrations of TSH, T4, T3, and PRL were compared with levels in six control ewes. All TRH-immunized ewes produced antibodies, which were maintained by booster immunizations throughout the study period. Effects on plasma contractions of immunoassayable TSH were slight and inconsistent, but there was a clear reduction in levels of T4 and T3 in the blood of the TRH-immunized ewes, although detectable amounts of the hormones were always present. The seasonal rises in PRL concentrations during the summer months and during pregnancy and lactation still occurred in the TRH-immunized ewes, although there was an indication that levels were slightly lower. Stimulation of the hypothalamic-pituitary system by subjecting the animals to heat stress caused a rise in plasma PRL concentrations in both groups, but this effect was significantly less in the TRH-immunized ewes. After the administration of metoclopramide, during suckling, and during estrus, PRL levels rose in both groups. Although the mean concentration of circulating PRL seemed lower in each instance in the TRH-immunized ewes, there was not a signicant difference. There was no difference in the time of onset of the breeding season, estrous cycle length, or the time of onset of estrous behavior in the TRH-immunized ewes. All six controls and four of the six TRH-immunized ewes became pregnant and delivered normal offspring. The marked reductions in plasma thyroid hormone concentrations in TRH-immunized ewes confirm that TRH is an important hypothalamic stimulator of TSH and, thus, thyroid function. In contrast, the absence of any major influence of TRH immunization on PRL levels in the different physiological situations suggests that it does not have an obligatory role in the control of PRL release. However, since the thyroid hormones were still present in low amounts in TRH-immunized ewes, it remains possible that the persistence of PRL secretion resulted from the presence of small amounts of biologically active TRH. In addition, adaptation of other hypothalamic control mechanisms for PRL release could occur, minimizing the effects of TRH neutralization. This together with reduced PRL response to acute stimuli mean that the possibility that TRH plays a minor role in PRL release cannot be excluded.

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