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A study was conducted to validate the previously reported growth response to cholecystokinin octapeptide (CCK-8) immunization in barrows and was extended to include gilts. Group-penned barrows and gilts were used to represent conditions in the swine industry. Thirty-two animals, 19 barrows and 13 gilts, were randomly assigned by sex to four pens and two treatments. The control groups were immunized with human serum globulin (hSG). The treated groups (CCK) were immunized with the C-terminal octapeptide of cholecystokinin conjugated to human serum globulin. Specific binding of CCK-8 was confirmed at 29 d after the primary inoculation. Antisera titers were highly variable throughout. The mean titer reached a peak on d 57 and then declined. Body weight gains during the last 49 d, the period during which titers were expressed, were compared by ANOVA. The treatment effect on gain was significant (P = .018); the sex effect approached significance (P = .071); the treatment x sex interaction effect was not significant (P = .82). Least squares mean gain of the CCK group was 8.4% greater than of the hSG group, 41.4 vs 38.2 kg, respectively. A significant linear regression coefficient for gain vs antisera titer was obtained for barrows (P = .03; r2 = .44) but not for gilts. Several carcass variables showed trends similar to that of BW gain, but the treatment effects were less robust (P < .05 to .10). These results generally confirm the findings of the previous study; CCK-8 immunization stimulated growth of barrows by 7.5% in the present and by 10.8% in the previous study.(ABSTRACT TRUNCATED AT 250 WORDS)

Eighty gilts were utilized to determine whether zeranol implants could maintain hCG-induced corpora lutea (CL) in peripubertal gilts and to examine the effects of a Zeranol implant on fetal development. Crossbred gilts (171+/-0.3 days of age, 109.1+1.4 kg) were blocked by weight and ancestry to control (n=40) or treatment (n=40) groups. To induce ovulation and CL maintenance, treated gilts received 500 IU of hCG i.m. and a Zeranol ear implant (Ralgro, 36 mg; day 0). All gilts were checked once daily for estrus with a mature boar from days 3-58 of the experiment. On day 42, treated gilts received two 10 mg injections of Lutalyse (PGF(2)alpha) spaced 6 h apart. Treated gilts not displaying estrus within 7 days of PGF(2)alpha received two additional 10 mg of PGF(2)alpha spaced 6 h apart on day 49. On days 44-58, gilts detected in estrus were inseminated twice, 24 h apart with pooled semen via AI. Blood samples were obtained on days 0, 7, 18 and 42 and analyzed for serum progesterone (P(4)). Bred gilts were slaughtered on days 58-62 of gestation. Ovulation, as determined by serum concentrations of P(4) on day 7 of the experiment, was induced by hCG in 79.5% of treated gilts. Zeranol implants, however, failed to increase (P0.05) the proportion of gilts available for breeding (treated, 21/39; control, 18/40). Of gilts inseminated on days 44-58, 16/21 treated gilts and 16/18 control gilts were pregnant at slaughter on days 58-62 of gestation. Number of fetuses (7.5 versus 12), fetal weight (83 versus 121 g), fetal length (117 versus 132 mm) and fetal survival (45% versus 78%) were reduced (P0.001) by Zeranol implants. These data indicate that treatment of peripubertal gilts with a 36 mg Zeranol implant did not increase the proportion of gilts available for breeding while causing deleterious effects upon the fetuses.

The role of endogenous opioids in controlling luteinizing hormone (LH) secretion was studied by injecting the opioid antagonist naloxone into intact and ovariectomized ewes that were treated with estradiol-17 beta (E2) and progesterone (P4). The existence of a naloxone-reversible inhibition of LH release was examined in five experiments using a total of 52 mature ewes. Naloxone at a dosage of 1 mg/kg disinhibited release of LH and abruptly increased serum concentrations of LH in a variety of experimental models. This naloxone-reversible inhibition of LH secretion was apparent in all experimental models that involved P4-induced inhibition of basal LH secretion but not in one model in which P4 inhibited the LH surge. Specific effects of E2 on naloxone-reversible inhibition of LH varied among experimental models. When prolonged administration of P4 alone appeared to lose its LH-inhibitory potency, E2 restored inhibition of LH as well as the naloxone-reversible state. Whenever E2 acted synergistically to suppress basal LH secretion in models involving brief (5 d) exposure to P4, E2 appeared to antagonize the naloxone-reversible state. In summary, P4-induced suppression of LH secretion appeared to be mediated by endogenous opioids, but the apparent interaction of E2 and opioids in LH suppression varied among experiments.

Thirty beef cows, approximately 3 yr of age, were randomly assigned to be slaughtered on d 7, 14, 28, 42 or 56 postpartum. Each cow suckled one calf until slaughter. Data from cows slaughtered on d 42 and 56 were pooled and further classified as anestrous or cyclic based on the presence of a corpus luteum and elevated serum concentrations of progesterone at slaughter. Specific binding of [3H]naloxone (3H-NAL) to homogenates of tissue from hypothalamus (HYP), preoptic area (POA) and basal forebrain (BF) was assessed using multiple-point Scatchard analyses. Nonspecific binding was estimated in the presence of 10(-6) M naloxone. Separation of bound from free 3H-NAL was achieved by centrifugation at 20,000 X g. Concentration (fmol/mg original tissue wet wt) of 3H-NAL binding sites in POA tissue was higher (P less than .05) on d 28 postpartum in anestrous cows than in cyclic cows on d 42 + 56 postpartum (2.58 +/- .32 vs 1.58 +/- .10). When all anestrous cows were compared with cyclic cows, concentrations of 3H-NAL binding sites in POA tissues and in BF tissue were higher (P less than .05) in anestrous cows (anestrous POA, 2.12 +/- .17, cyclic POA, 1.58 +/- .10; anestrous BF, 2.94 +/- .41, cyclic BF, 2.19 +/- .16). Compared across brain regions for all cows, the concentration of specific binding sites for 3H-NAL was greater (P less than .01) in BF (2.5 +/- .2) than in POA (1.9 +/- .1) and greater (P less than .01) in POA than in HYP (1.5 +/- .1).(ABSTRACT TRUNCATED AT 250 WORDS)