Central Nervous System Regions Involved in the Estrogen-Induced Afternoon Prolactin Surge. I. Lesion Studies*

Abstract

CNS regions were examined in long-term ovariectomized rats to determine if they are involved in the estrogen-induced afternoon surge in plasma PRL. Adult female rats were ovariectomized 2-3 wk before bilateral radiofrequency or electrolytic lesions of the brain were placed on day 0. In short-term lesion studies, catherizations and s.c. injections of polyestradiol phosphate (PEP) were done after the lesion was made; blood sampling was performed on day 2, 3, 4 or 6. In long-term lesion studies, the catheterization and PEP injection were done on day 21; blood was collected on day 28. In short-term experiments, extensive lesions in the medial preoptic area/suprachiasmatic nuclei (MPO/SCN) completely blocked the PEP-induced afternoon PRL surges sampled on days 2, 3, 4 and 6, while bilateral lesions in the corticomedial amygdala (CMA) had no effect. Discrete bilateral lesions of either MPO or SCN eliminated the afternoon PRL surge on day 6. Discrete, yet complete, lesions of the ventromedial nuclei of the hypothalamus also blocked the PRL surge; lesions in the dorsomedial neclei of the hypothalamus increased the magnitude of the afternoon PRL surge. In long-term studies, lesions of the CMA delayed and attenuated the PEP-induced PRL surge and lesions of the stria terminalis for 4 wk had a similar effect. As in the short-term lesion studies, long-term lesions of the MPO/SCN eliminated the daily rhythm of PRL secretion, although small sporadic rises in plasma PRL levels could be observed throughout the sampling period. Apparently, structural integrity of the MPO/SCN and ventromedial hypothalamic nuclei is essential for the estrogen-induced afternoon PRL surge; destruction of the dorsomedial hypothalamic nuclei can increase the magnitude of the afternoon PRL surge; the CMA is not essential for induction of the PRL surge even though removing its neural input to the hypothalamus for an extended period can delay the onset of and suppress the magnitude of hormone release.