Pulsatile administration of gonadotropin-releasing hormone agonist to gilts actively immunized against gonadotropin-releasing hormone.

Sexually mature gilts (n = 20) were actively immunized against GnRH. Primary and booster immunizations of GnRH conjugated to bovine serum albumin induced production of antibodies in all gilts. Nineteen of the gilts became acyclic with suppressed concentrations of gonadotropins and estradiol. Intravenous challenges with 100 micrograms GnRH and 5 micrograms D-(Ala6, des-Gly-NH2(10)) ethylamide GnRH (a GnRH agonist that did not cross-react with antibodies produced by the gilts) caused release of LH and FSH, indicating maintenance of secretory capacity of pituitary gonadotropes in the immunized animals. Gilts were given 100 ng GnRH agonist at 2-h intervals for 72 h (n = 4) or 144 h (n = 10) or did not receive agonist (n = 5). Blood samples were taken every 6 h, and detectable concentrations of LH were observed in 42% and 52% of samples taken from gilts treated with or without agonist. In contrast, serum concentrations of FSH and estradiol were undetectable. Reproductive tracts and anterior pituitaries were taken from gilts at the conclusion of pulsatile administration of GnRH agonist or at 144 h for controls. Pituitary concentration of LH and FSH, uterine wet and dry weight, and size of the uterus were similar among groups. Paired ovarian weights for treated gilts pulsed with GnRH agonist for 72 h were heavier (P less than .05); however, ovaries from all immunized gilts were atrophied without follicular structures.(ABSTRACT TRUNCATED AT 250 WORDS)