A single injection of 17β-estradiol into castrated male or female rats results in an initial decrease in plasma concentrations of LH and pituitary responsivenesses to LHRH, followed by a rapid return to normal or slightly elevated values. Under such experimental conditions, no acute change of binding of [125I-labeled D-Ser(TBU)6]LHRH ethylamide to anterior pituitary homogenate could be observed. Moreover, the self-priming effect of LHRH, as illustrated by a 10-fold increase in the LH response to a second injection of LHRH in the afternoon of proestrus, is accompanied by a 40% loss of pituitary LHRH receptors. During the estrous cycle, a 100% increase in pituitary LHRH receptors is already found on diestrus II, while the maximal LH responsiveness to LHRH occurs later, namely on the afternoon of proestrus. The present findings of a dissociation between changes in LHRH receptor levels and LH responsiveness to the neurohormones suggest that postreceptor events play a predominant role in the control of gonadotropin secretion by sex steroids and LHRH itself. Moreover, LHRH can cause an acute down-regulation of its own receptor in the anterior pituitary gland.
|Number of pages||7|
|Publication status||Published - 1981|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism