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Regulation Versus Modulation in GnRH Receptor Function

Serum luteinizing hormone (LH) concentration after exposure to gonadotropin-releasing hormone (GnRH) indicates that an instantaneous increase occurs in the rate of release of LH directly from the anterior pituitary, as measured dynamically during superfusion in vitro. On the other hand, estra-diol-17β (E2) alone shows no such instantaneous effect on LH release rate (at least for the first four hours), in either physiologic or pharmacologic concentrations. At the same time, brief (ten to 30 minute) exposure of isolated anterior pituitary plasma membranes to physiologic concentrations of E2 significantly alters the binding of a fully biologically active 125[-GnRH to its plasma membrane receptor protein. In order to characterize the effect of E2 on GnRH binding further, we preincubated dispersed bovine anterior pituitary cells for six hours in the presence or absence of physiologic concentrations of E2 (10−10M). Following preincubation in the presence of E2, the cell suspension was incubated for 30 minutes with physiologic concentrations (5 x 10−11 – 5 x 10−10M) of a fully biologically active 125[-GnRH. The treatment, at least, doubled the number of biologically important high affinity GnRH binding sites (Kd's = 7.5 x-10−11 – 4.5 x 10−10M), and changed the binding capacity of some of the binding sites up to three fold, which altered the cooperativity of GnRH-receptor interaction. Thus, the interaction of E2 with GnRH at the level of GnRH receptor is mandatory for the short-term pituitary effect of E2 on LH release in vitro and in vivo. At least, during the initial exposure of anterior pituitary cells, GnRH and E2 function more as a controller and modulator, respectively.