ESTROGEN FEEDBACK NEEDED AT THE PARAVENTRICULAR NUCLEUS OR A2 TO SUPPRESS PULSATILE LUTEINIZING-HORMONE RELEASE IN FASTING FEMALE RATS

The feedback sites of estrogen within the hypothalamus and lower brain stem involved in the suppression of pulsatile LH secretion during 48- h fasting were examined in ovariectomized rats with local estradiol (E (2)) implants. The animals were ovariectomized and immediately implant ed stereotaxically with stainless steel cannula containing crystal E(2 ) diluted 10 times with crystal cholesterol into the medial preoptic a rea, paraventricular nucleus (PVN), arcuate nucleus (ARC), locus cerul eus, or A1 or A2 region of the brain. Five days later, animals were de prived of food for 48 h, and blood samples were collected every 6 min for 3 h. Animals were immediately refed for 45 h and bled again as des cribed above. Changes in the mean LH concentrations over the 3-h sampl ing period and the frequency and amplitude of LH pulses were determine d by calculating the differences in these parameters between the first and second blood samplings in each animal. Fasting significantly lowe red mean LH concentrations in animals implanted with E(2) in the A2. T he more potent suppression of pulsatile LH release during fasting was found in rats with E(2) implants in the PVN: the mean LH concentration s and LH pulse frequency were significantly reduced by fasting in this group. In the animals with E(2) implants in the medial preoptic area, ARC, locus ceruleus, or A1, 48-h fasting did not induce any significa nt changes in LH pulse parameters compared to those in cholesterol-imp lanted controls. A decrease in LH pulse amplitude was apparent in refe d rats as well as fasted animals only when E(2) was implanted in the A RC. These results suggest that the feedback action of estrogen at the PVN and/or A2 is required for fasting-induced suppression of pulsatile LH release, as opposed to the so-called negative feedback action of e strogen, which tonically suppresses LH release in nonfasting rats.