Effect of Median Eminence Lesions on [3H]Estradiol Binding in the Anterior Pituitary and Hypothalamus*
Open Access
- 1 November 1979
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 105 (5) , 1152-1157
- https://doi.org/10.1210/endo-105-5-1152
Abstract
The binding and uptake of [3H]estradiol were studied in the anterior pituitary (AP) and hypothalamus of ovariectomized rats which were subjected to electrolytic destruction of the median eminence or to sham operation. As expected, serum PRL levels were markedly increased while LH was low in the lesioned rats. [3H]Estradiol binding in vitro by cytosol from the AP was decreased from a control value of 59.7 ± 6.2 to 36.9 ±6.1 fmol/mg protein in rats studied 8–10 days after placement of the lesion (P < 0.025). A time-course study, performed at various times after the lesion, indicated that binding of [3H]-estradiol in the AP was lower than normal when measured at 1 h and 1, 7, and 21 days. These changes were accompanied by increments in serum PRL throughout the experiment. Scatchard plot analysis of the binding data demonstrated a decreased binding capacity after median eminence lesion and an association constant in the range of the control AP. In contrast to the findings with the AP, median eminence lesion had no effect on [3H]estradiol binding in cytosol of hypothalamus. Intravenous administration of [3H]estradiol to control rats and rats lesioned 8 days previously demonstrated a significant lower uptake of radioactivity in the latter group in both AP and hypothalamus in vivo, regardless of whether results were expressed as the tissue to cortex ratio or as disintegrations per min/100 mg. The rates of [3H]glycine incorporation into proteins measured in incubated AP or hypothalamus were similar in controls and in rats with median eminence lesions, indicating that the decrement in binding or uptake was not due to an inhibition of total protein synthesis. These results suggest that estrogen receptors in the AP may be influenced by the brain, either by a direct trophic action of the hypothalamus or indirectly by regulation of serum PRL levels.Keywords
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