No abstract

Testes function, feedlot performance, and carcass traits were evaluated in bulls actively immunized against gonadotropin-releasing hormone (GnRH) at different ages. Bull calves were randomly assigned to one of seven treatment groups (n = 15 calves/group). Calves were unimmunized (Group 1), immunized at 1.5, 4, 7, or 12 mo of age with a GnRH-keyhole limpet hemocyanin (KLH) conjugate (Groups 2 to 5, respectively), or castrated at 4 mo of age (Groups 6 and 7). Immunized bulls did not receive a secondary, or booster, immunization. Calves in group 6 received Synovex-C at castration and Synovex-S at weaning and feedlot entry. Anti-GnRH titer was evident at slaughter in all immunized bulls. However, the final immune response of bulls immunized at 1.5 mo was significantly lower than the response of bulls immunized at later stages of development. Final scrotal circumference and testis weight in bulls immunized at 4, 7, or 12 mo of age were significantly reduced relative to unimmunized bulls. The final live weight, feedlot gain, and carcass weight of immunized and unimmunized bulls did not differ (P > .05) from the same parameters in steers implanted with Synovex. Longissimus muscle area, marbling score, and backfat thickness did not differ between immunized and unimmunized bulls. The sex class score of the carcasses of immunized bulls did not differ from the score of steer carcasses. In contrast, a significantly higher proportion of carcasses from unimmunized bulls graded as bullock carcasses. Taken together, these data indicate that a single immunization against GnRH at 4 to 12 mo of age results in significant attenuation of testicular growth in bulls. These data also demonstrate that immunization against GnRH reduces the masculinity of carcasses from bulls, but does not affect feedlot performance, longissimus muscle area, marbling score, or backfat thickness. These results suggest that single immunization with the GnRH-KLH conjugate may have practical utility as a noninvasive alternative to surgical castration in management of beef cattle.

The pattern of GnRH-like stimuli capable of inducing follicular growth, ovulation, and luteal function was evaluated in ewes passively immunized against GnRH. The estrous cycles of 30 regularly cyclic sheep were synchronized using vaginal pessaries impregnated with a synthetic progestogen. Animals were passively immunized against GnRH (groups 2-5, n = 6) or the carrier protein, keyhole limpet hemocyanin (KLH; group 1, n = 6), at the time of pessary removal (PR). Circhoral delivery of saline (groups 1, 2, and 5) or low amplitude GnRH agonist (des-Gly10 GnRH ethylamide [100 ng/hourly pulse]; groups 3 and 4) was initiated at PR and continued for 3 (groups 4 and 5) or 12 days (groups 1-3). In groups 4 and 5, the amplitude of the GnRH-like stimulus was increased to 800 ng/hourly pulse (stimulus-shift) during the 24-h period beginning 72 h after PR. The amplitude of the hourly stimulus was adjusted to 100 ng/pulse 96 h after PR and continued at that level to Day 12. The endocrine changes associated with follicle growth and maturation (serum concentrations of estradiol [E2] above 10 pg/ml), ovulation (surge-like secretion of LH and FSH), and normal luteal function (serum concentrations of progesterone [P] above 2 ng/ml) were evident in ewes passively immunized against KLH (group 1). In this group, the preovulatory surge of gonadotropins was noted 48.7 +/- 1.2 h after PR. These endocrine events were blocked by passive immunization against GnRH (group 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Two trials were conducted to examine reproductive function and feedlot performance by heifers after active immunization against GnRH. In trial 1, heifers were not immunized or were immunized with one of three doses of a GnRH-KLH (keyhole limpet hemocyanin) conjugate in Freund's complete adjuvant. Antibodies against GnRH were not detectable in non-immunized heifers (n = 9). However, antibodies against GnRH were noted in all immunized animals (n = 30) within 8 wk of primary immunization; anti-GnRH antibody concentrations were at a maximum 16 to 20 wk after immunization. This increased anti-GnRH titer was associated with a decreased serum concentration of progesterone. Ovarian and uterine weight and tissue concentrations of LH and GnRH receptor were reduced (P less than .05) by immunoneutralization of GnRH. Similarly, immunization against GnRH reduced (P less than .05) weight gain during feedlot confinement. In trial 2, feedlot performance after insertion of anabolic steroid implants (Synovex H) was evaluated in non-immunized heifers (n = 15), heifers actively immunized against GnRH-KLH (n = 15) or KLH alone (n = 15), or non-immunized heifers treated with melengestrol acetate (MGA; n = 15). Serum concentrations of progesterone were depressed in anti-GnRH and MGA-fed groups, but ovarian and uterine weights were depressed (P less than .05) only in heifers immunized against GnRH. Total weight gain and gain during the final 4 wk of confinement did not differ (P greater than .05) among groups with steroid implants. The GnRH-KLH conjugate is an effective immunogen in heifers, leading to suppression of reproductive activity. The depression of weight gain that attends development of anti-GnRH titers may be reversed by use of implants that contain anabolic steroids.

The effects of estradiol (E2) and E2 withdrawal on tissue concentrations of GnRH receptor mRNA were assessed in orchidectomized sheep (wethers). Wethers received E2 (in 20% ethanol-saline [vehicle]) by continuous infusion at rates of 0.31, 1.25, 5, or 20 micrograms/h (n = 12 animals per group). Control animals received vehicle alone. Anterior pituitary tissue was collected at the end of the 48-h infusion period. Steady-state levels of GnRH receptor mRNA were quantified by solution hybridization. Tissue levels of mRNA were significantly increased above control levels (0.5 +/- 0.1 pg/microgram RNA) by E2 infusion at 1.25 micrograms/h (1.4 +/- 0.2 pg/microgram RNA). Maximal tissue concentrations of GnRH receptor mRNA were induced by E2 delivery at 5 micrograms/h (2.4 +/- 0.3 pg/micrograms RNA). In a second study, wethers (n = 6 animals per group) received 5 micrograms E2/h for 24 h. Pituitary tissue was collected at the end of the infusion period or at 12, 24, or 48 h after cessation of E2 delivery. Infusion of E2 induced a 6-fold increase in GnRH receptor mRNA (0.4 +/- 0.1 and 2.9 +/- 0.6 pg/micrograms RNA in control and E2-treated groups, respectively). Cessation of E2 delivery resulted in rapid reduction in steady-state levels of GnRH receptor mRNA. Tissue concentrations of receptor mRNA returned to pretreatment levels within 12 h of E2 withdrawal (0.6 +/- 0.1 pg/microgram RNA). In a third study, the concentration of GnRH receptor mRNA was determined in pituitary tissue collected during preovulatory surge-like secretion induced in E2-infused wethers by episodic delivery of high-amplitude GnRH (1600 ng GnRH per hourly pulse). Estradiol (5 micrograms/ml in 10% ethanol-saline) was delivered as a continuous infusion. Episodic delivery of GnRH was initiated 24 h after E2 infusion was begun, and concurrent administration of E2 and episodic GnRH was continued to slaughter. Anterior pituitary tissue was collected at 0, 3, 6, 12, or 24 h after beginning circhoral delivery of GnRH (n = 6 wethers per group). As noted above, continuous infusion of E2 for 24 h significantly increased tissue concentrations of GnRH receptor mRNA. However, steady-state levels of GnRH receptor mRNA were returned to pretreatment levels after 3 h of circhoral delivery of GnRH (0.4 +/- 0.1 pg/microgram RNA). Taken together, these data demonstrate that physiological concentrations of E2 increase steady-state levels of GnRH receptor mRNA in a dose-dependent manner. In addition, continued estrogenic support is required to maintain enhanced tissue concentrations of GnRH receptor mRNA. Finally, high-amplitude GnRH stimulation induces down-regulation of tissue levels of GnRH receptor mRNA. These data suggest that the dynamic changes in tissue concentrations of GnRH receptor mRNA during the periovulatory period may be due to the inductive effects of gonadal steroids from the developing follicle and to the combined suppressive effects of the increased GnRH stimulation and E2 withdrawal that are associated with the gonadotropin surge.