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Endocrinology, Vol 135, 870-875, Copyright © 1994 by Endocrine Society

ARTICLES

Estrogen feedback needed at the paraventricular nucleus or A2 to suppress pulsatile luteinizing hormone release in fasting female rats

S Nagatani, H Tsukamura and K Maeda
Nagoya University School of Agricultural Sciences, Japan.

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 (E2) implants. The animals were ovariectomized and immediately implanted stereotaxically with stainless steel cannula containing crystal E2 diluted 10 times with crystal cholesterol into the medial preoptic area, paraventricular nucleus (PVN), arcuate nucleus (ARC), locus ceruleus, or A1 or A2 region of the brain. Five days later, animals were deprived 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 described above. Changes in the mean LH concentrations over the 3-h sampling period and the frequency and amplitude of LH pulses were determined by calculating the differences in these parameters between the first and second blood samplings in each animal. Fasting significantly lowered mean LH concentrations in animals implanted with E2 in the A2. The more potent suppression of pulsatile LH release during fasting was found in rats with E2 implants in the PVN: the mean LH concentrations and LH pulse frequency were significantly reduced by fasting in this group. In the animals with E2 implants in the medial preoptic area, ARC, locus ceruleus, or A1, 48-h fasting did not induce any significant changes in LH pulse parameters compared to those in cholesterol-implanted controls. A decrease in LH pulse amplitude was apparent in refed rats as well as fasted animals only when E2 was implanted in the ARC. 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 estrogen, which tonically suppresses LH release in nonfasting rats.


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