Evidence for the dependence of serum luteinizing hormone surge on a transient, enhanced secretion of gonadotropin-releasing hormone from the hypothalamus.
Data that a substantial, transient release of gonadotropin-releasing hormone (GnRH) from the hypothalamus is a prerequisite for the serum luteinizing hormone (LH) surge are presented. Ovariectomized rats, in which daily afternoon LH peaks can be induced by estradiol benzoate (EB), were used as the experimental model. These rats present a homogenous, synchronized population having low hypothalamic stores of GnRH, thus facilitating detection of small physiological fluctuations in the levels of hypothalamic GnRH. Blockade, by Nembutal administration, of the serum LH surge on 2 consecutive afternoons results in elevated GnRH levels in the hypothalamus (1.79 ng in blocked rats vs 0.94 ng in controls). Abolition of LH secretion by administration of antiserum to GnRH, unlike the Nembutal blockade, does not affect GnRH levels. These results indicate that the afternoon LH surge is dependent on a transitory, enhanced release of GnRH from the hypothalamus, reflected by a depletion of GnRH stores.
D000818:Animals; D002369:Castration; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000276:immunology / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007106:Immune Sera / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000097:blood*; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D013997:Time Factors
D007106:Immune Sera; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D007986:Luteinizing Hormone; D010424:Pentobarbital