Cellular mechanisms of acute estrogen negative feedback on LH secretion: pituitary responsiveness to LHRH and estradiol receptor kinetics in the pituitary, preoptic hypothalamic area, and the caudal hypothalamic area of the rat brain.

In order to examine the cellular mechanisms by which estradiol (E2) exerts its acute negative feedback upon luteinizing hormone (LH) secretion, a temporal correlation was made among serum LH concentrations, pituitary responsiveness to luteinizing hormone-releasing hormone (LHRH), and the translocation of E2 to nuclear (NER) receptors of the pituitary (PIT), preoptic hypothalamic area (POA), and the caudal hypothalamic area (HYP). Rats on diestrous day 1 were ovariectomized (OVX) and killed 10 days later. LH and LHRH were measured by RIA. NER was measured by an exchange assay. Serum LH increased 10-12-fold 10 days following OVX as compared to diestrous controls. The injection of estradiol benzoate (Eb, 20 microgram in corn oil/rat, sc) did not affect LH concentrations at 30 min but decreased serum LH at both 60 and 180 min following its administration. Pituitary responsiveness to LHRH (measured as the increase in LH 10 min after iv injections of 100 ng LHRH/rat) was not altered at 60 min but was significantly decreased 180 min following Eb injection. Thus, serum LH decreased prior to a detectable alteration in pituitary responsiveness to LHRH. Translocation of E2 receptors to NER of the HYP and PIT began 60 min following Eb injection and was maximal at 180 min. In contrast, translocation of E2 receptors in the POA was maximal at 60 min, and had recovered to control values 180 min following Eb administration.(ABSTRACT TRUNCATED AT 250 WORDS)