Response to luteinizing hormone releasing hormone in postpubertal boars with large testes

The objective of the present study was to determine if postpubertal boars (12-13 months of age; 156 +/- 8 kg) with large testes had altered hypothalamic control of secretion of luteinizing hormone (LH). Seven boars with the highest estimated 150 d, paired testis weights from a line selected for large testes (769 +/- 60 g = mean weight of excised testes) and 8 boars from a control group (control, 544 +/- 20 g) were tethered in stalls and fitted with indwelling jugular catheters. Males were bled when they were intact, 14 days after castration and during administration of sodium pentobarbital anesthetic (subsequent to castration) to block secretion of endogenous LH-releasing hormone (LHRH). Blood samples were collected at 12-min intervals for 6 hr before and 1 hr after intravenous injection of LHRH in intact and castrated males. During anesthesia, LHRH was administered 4 times at 1-hr intervals and blood samples were collected every 6 min. All samples were analyzed for concentrations of LH and pooled samples were analyzed for concentrations of 17-beta estradiol (E2) and testosterone (T). In intact and castrated males, mean concentrations of LH, frequency and amplitude of pulses of LH, and concentrations of E2 and T were not different between boars of the two groups (P greater than .10). Response to exogenous LHRH was less (P less than .05) in intact males with large testes than in corresponding males from the control group (P less than .05). Fourteen days after castration, males that had larger testes before castration had less of a response to LHRH than males from the control group (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of luteinizing hormone in postpubertal boars with large testes

The objective of the present study was to investigate endocrine control of LH in postpubertal boars with large testes. Eight boars with the highest estimated paired testis weights from a line selected for large testes and nine boars from a line selected at random were used. Blood samples were collected over a 13-h period at weekly intervals for 4 wk. Samples were collected at 12-min intervals for 12 h before and 1 h after exogenous LHRH. Boars were bled when they were intact during the initial week. The second and third blood collections were 7 and 14 d after castration. The fourth bleeding occurred 7 d after exogenous 17 beta-estradiol (E2) replacement. In intact boars, mean LH was similar between boars from the two groups, but amplitude of pulses of LH was lower in intact boars with large testes than in boars from the control line. Maximum concentration of LH after administration of LHRH was less in boars with large testes than in boars from the control group. Seven days after castration, characteristics of LH measured did not differ between males from the two groups. However, 14 d after castration, amplitude of pulses of LH and maximum concentrations of LH after LHRH were less in males from the group with large testes than in males from the control group. After E2 administration, amplitude of pulses of LH tended to be lower in males from the group with large testes than in males from the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gonadal regulation of LH secretion in prepubertal bull calves

In the present study we examined the influence of castration and exogenous estradiol on pulsatile LH release during the transition from infancy to the prepubertal period of development. Bull calves were assigned to treatments (N = 5 treatment) at 6 weeks of age. Treatments consisted of intact controls, castrates and castrates receiving estradiol implants. Plasma LH response was monitored over 8 hr periods at 7, 8, 9, 10, 11 and 13 weeks of age. Castration alone did not alter LH concentrations, compared to controls until 10 weeks of age. At 10, 11 and 13 weeks, mean LH concentration and the number of LH pulses/8 hr period were greater (P less than .05) in castrates than in controls. In castrates with estradiol implants, mean LH concentration and the number of LH pulses/8 hr period were suppressed at all ages compared to controls and castrate treatments. These results indicate that LH release is not inhibited by gonadal factors from 6 to 9 weeks of age in the bull calf. However, estradiol negative feedback on LH secretion is evident during this same developmental period.     

Effects of estradiol-17 beta, naloxone and gonadotropin releasing hormone on postpartum secretion of luteinizing hormone in fall-lambing ewes

The interaction among exogenous estradiol-17 beta, naloxone and gonadotropin releasing hormone (GnRH) in the control of luteinizing hormone (LH) secretion was studied in intact postpartum ewes nursing their offspring. One-half of 30 fall-lambing ewes were implanted subcutaneously with an estradiol-17 beta containing Silastic capsule between postpartum d 1 and 12 which doubled their serum concentrations of estradiol (16.0 +/- .1 vs 8.4 +/- .1 pg/ml). Blood samples were collected from implanted and non-implanted ewes at 15-min intervals for 5 h on d 3, 8, 13, 20 and 28 postpartum. Pre-injection samples were collected for 1 h, and ewes were injected with saline, naloxone (NAL;1 mg/kg) or GnRH (100 micrograms/ewe). When averaged across all days and implant groups, serum LH in the three post-NAL samples was higher (P less than .05) than in the three pre-NAL samples (3.6 +/- 1.2 vs .6 +/- .2 ng/ml). Post-GnRH concentrations of serum LH were lower (P less than .05) in estradiol-implanted ewes than in non-implanted ewes on d 8 and 13, but there were no differences in any LH characteristics on d 20 and 28 after implant removal on d 12. In non-implanted ewes, serum LH responses to GnRH increased (P less than .05) eightfold from d 3 (3.8 +/- 1.4 ng/ml) to d 8 (31.6 +/- 1.4 ng/ml), remained elevated through d 20, but declined by d 28 (10.8 +/- 1.4 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of duration of photoperiod and hemicastration on growth and testicular and endocrine functions of boars

Yorkshire boars were used to evaluate the influence of duration of photoperiod and hemicastration on growth and testicular and endocrine functions. At 10 wk of age, 5 hemicastrate (HC) and 5 intact (I) boars were assigned to either 8 or 16 hr of light daily until 6 mo of age. Body weights were recorded biweekly throughout the experiment. Venous cannulae were placed in all boars at 6 mo of age, and serum was collected at 30 min intervals from 0800 to 2000 hr. Gonadotropin releasing hormone (GnRH) was infused at 2000 hr (50 micrograms) and at 2030 hr (250 micrograms), and samples of serum were collected until 2400 hr. The following day, all boars were castrated, and the weights and sperm content of the testes and epididymides were determined. At castration, all pigs were given implants containing testosterone. Two weeks later, pigs were again canulated, and serum was obtained at 15 min intervals for 2 hr. Growth of boars was not significantly affected by duration of photoperiod or number of testes. Duration of photoperiod did not affect weight or sperm content of testes or epididymides. Hemi-castrated boars had greater testicular (P less than .01) and capita-corpora (C-C) epididymal weights (P less than .05) and more testicular and C-C sperm (P less than .01) per testis. Neither average concentrations of luteinizing hormone (LH) nor number and amplitude of pulses of LH were affected by photoperiod treatment. However, HC boars had greater average concentrations of LH (P less than .05) than I boars (.71 +/- .05 vs .52 +/- .05 ng/ml). Hemicastrated boars in 16 hr light daily had greater concentrations of FSH in serum (P less than .05) than 8I, 8HC, and 16I boars. Intact and HC boars had similar concentrations of prolactin (PRL) and testosterone. Similarly, concentrations of PRL and testosterone were not affected by duration of photoperiod. Secretion of LH and testosterone after treatment with GnRH was not significantly affected by duration of photoperiod. In general, HC boars released more LH in response to GnRH treatment than I boars. Concentrations of LH were greater (P less than .05) in HC than I boars at .5, 1, 2, and 3 hr after GnRH and tended (P less than .10) to be elevated at 1.5, 2.5, 3.5 and 4 hr after GnRH. The FSH response to GnRH was greater (P less than .05) for 16HC than 8I, 8HC, or 16I boars.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of chronic gonadotropin-releasing hormone agonist treatment on serum luteinizing hormone and testosterone concentrations in boars.

Mature boars were subjected to chronic treatment with a gonadotropin-releasing hormone (GnRH) agonist, goserelin (D-Ser[But]6, Azgly-NH210), and serum luteinizing hormone (LH) and testosterone concentrations were measured. Ten sexually mature boars were randomly assigned to treatment (n = 5) or control (n = 5) groups. On day 0, boars were implanted sc (day 0) with 2 GnRH agonist implants (1 mg of GnRH/implant) or sham implants. Blood samples were collected at 12-hour intervals on days -2 and -1, at 6-hour intervals on days 0 through 4, and at 12-hour intervals on days 5 through 8. In addition, blood samples were collected at 15-minute intervals for 6 hours on days -1, 0, 4, and 8. Serum testosterone and LH concentrations were determined by radioimmunoassay. Maximal LH (7 +/- 1 ng/ml) and testosterone (26 +/- 3 ng/ml) concentrations were observed at 5 and 18 hours, respectively, after GnRH agonist treatment. Subsequently, LH and testosterone concentrations decreased to pretreatment values (0.3 +/- 0.1 ng/ml and 1.8 +/- 0.4 ng/ml, respectively) by 24 and 48 hours, respectively, after GnRH agonist implantation. Few differences in the characteristics of pulsatile LH release were observed between the groups. Testosterone and LH concentrations in samples collected at 6- and 12-hour intervals and pulsatile LH release did not change after sham treatment of control boars. Whereas previous reports indicated that chronic GnRH administration suppressed serum LH and testosterone concentrations in rams, rats, and dogs, our results indicate that chronic GnRH agonist treatment induced transitory increases, without subsequent suppression, in LH and testosterone concentrations in mature boars.     

Influence of the ovary and suckling on luteinizing hormone response to naloxone in postpartum beef cows

The influence of the suckling stimulus and ovarian secretions on LH response to naloxone was studied in 16 postpartum anestrous beef cows that were assigned randomly to one of four groups (n = 4/group): intact suckled (IS), intact nonsuckled (IN), ovariectomized suckled (OS) or ovariectomized nonsuckled (ON). Ovariectomy (OS + ON) and calf removal (IN + ON) were performed on d 2, 3 or 4 after parturition. Jugular venous blood was collected at 15-min intervals for 4 h before and 4 h after administration of naloxone (1 mg/kg BW, i.v.) on d 14 and d 28 after parturition. Gonadotropin-releasing hormone (5 micrograms, i.v.) was given 3 h after naloxone. Both IN and OS increased (P less than .05) mean pretreatment LH above IS values (mean +/- SE, ng/ml; IS 1.6 +/- .1 vs IN 2.5 +/- .3 and OS 2.7 +/- .4; P less than .01), whereas ON increased (P less than .01) LH (3.7 +/- .3 ng/ml) even further. Mean LH increased (P less than .05) after naloxone administration in all treatment groups. However, magnitude of this response was variable and dependent on ovarian status. Amplitude of the naloxone-induced LH response was greater (P less than .05) for ovariectomized (5.9 +/- 1.1 ng/ml) than for intact groups (2.7 +/- .5 ng/ml). Gonadotropin-releasing hormone increased mean LH concentrations in all groups. We suggest that ovarian secretions and the suckling stimulus contribute to endogenous opioid inhibition of LH during the postpartum interval.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of prepubertal consumption of zearalenone on puberty and subsequent reproduction of gilts

Forty-eight prepubertal gilts (178.7 +/- 4.1 d; 94.2 +/- 4.1 kg), 16 in each of three trials, were assigned randomly to receive 0 (C) or 10 ppm zearalenone (Z) daily in 2.5 kg of a 14% protein finishing ration for 2 wk. Blood samples were collected at 20-min intervals for 4 h 1 wk after the start of the experiment and 1 wk after Z was withdrawn. Two weeks after Z was withdrawn, gilts were exposed to mature boars 15 min per day for 3 wk. Gilts in estrus were mated to two different boars 12 h apart. Twice each week, blood was sampled and analyzed for progesterone to establish age of puberty. Age at puberty differed (P = .008) among replicates but was similar (P = .13) between Z and C gilts within each replicate. Mean serum concentrations of LH were suppressed (P = .025) during consumption of Z (.25 vs .42 ng/ml) but were similar (P = .16) to concentrations in C gilts 1 wk after Z was withdrawn (.35 vs .45 ng/ml). Frequency and amplitude of LH secretory spikes did not differ (P greater than .50) between Z and C gilts during either sampling period. Mean serum concentrations of FSH were similar (P = .25) between Z and C gilts. Number of corpora lutea and live fetuses were similar (P = .29 and P = .94, respectively) between Z and C gilts. Fetal weights were greater (P = .025) and crown to rump length tended to be greater (P = .10) in fetuses from Z gilts.(ABSTRACT TRUNCATED AT 250 WORDS)     

Performance of male pigs immunized against GnRH is related to the time of onset of biological response

In this study, the performance of male pigs immunized against GnRH was determined in relation to the onset of their biological response to the immunization. Pigs were immunized at 9 and 17 wk of age and were housed in a pen together with both a surgically castrated and an intact boar littermate. Feed intake was restricted to 2.8 to 3.2 times maintenance requirement for energy. Animals were weighed weekly and slaughtered at 108 kg BW. Depending on the time of onset of the response after immunization in terms of biological effects, immunized pigs were retrospectively grouped into two categories. One category consisted of the immunized pigs, which had undetectable or low levels of LH and testosterone at the time of booster immunization-known as "early" responding immunocastrates (E-IM, n = 8), whereas the "late" responding immunocastrates (L-IM, n = 7) had substantial LH and testosterone levels at that time. This dichotomy of the response to immunization also was reflected in testis weight, with 17 g and 40 g for E-IM and L-IM pigs, respectively. At slaughter, testis size and weight were reduced (P < 0.001) in the immunocastrated pigs as compared to the intact boars. Androstenone concentrations in backfat of all immunocastrated pigs were undetectable. Growth performance (i.e., ADG and feed efficiency [FE, g gain/kg feed]), was better in boars and L-IM pigs than in surgical castrates and E-IM pigs (P < 0.05). Average daily gain and FE did not differ between E-IM pigs and the surgical castrates, but intact boars performed better than L-IM (P < 0.02). There were no significant differences in carcass quality (backfat thickness and meat percentage) between boars and surgical castrates at slaughter. However, for both characteristics L-IM pigs and intact boars performed better (P < 0.03) than E-IM pigs. Thus, growth performance in L-IM is better than in either E-IM or surgical castrates.     

Effects of season and estradiol-17 beta on luteinizing hormone release in ovariectomized sows.

This study examined the ability of estradiol-17 beta (E2) to suppress LH release in the sow during different months of the year. Six chronically ovariectomized sows were fitted with vena caval cannulas (d 0) and blood samples were collected at 6-h intervals for 6 d. Sows were treated s.c. with E2 capsules (24 mg of E2/275 kg of BW) at d 3. Additional blood samples were collected at 15-min intervals for 8 h on d 2 and 5. After each 8-h frequent sampling period, sows were treated i.v. with GnRH at .5 microgram/kg of BW, and blood samples were collected at 10-min intervals for 3 h. The protocol was repeated at monthly intervals for 13 mo. Luteinizing hormone concentrations were determined for all serum samples, and E2 concentrations were quantified in samples collected at 6-h intervals. Data were analyzed by split-block analyses of variance. Serum E2 concentrations increased (P less than .001) from 5.0 +/- .3 pg/ml before E2 treatment to 26.0 +/- .2 pg/ml after E2 treatment. The interval from GnRH administration to peak LH concentration was shorter (P less than .001) before E2 treatment than after E2 treatment (28.7 +/- 2.2 vs 71.0 +/- 2.2 min). It was evident that baseline LH, mean LH, pulse frequency, and pulse amplitude and LH release after GnRH administration failed to demonstrate seasonal changes. In summary, LH release was suppressed after treatment with E2 and was affected minimally by month of the year. In addition, E2 inhibitory effects of LH release included hypothalamic and anterior pituitary sites of action.     

Changes in the pituitary-gonadal axis associated with puberty in Holstein bulls

The temporal pattern of the endocrine changes associated with puberty were studied using 52 bulls born in October or April. Blood samples were taken weekly and at 30-min intervals for 5 h every 4-wk. Bulls were castrated at one of six 4-wk intervals between 12 and 32 wk and blood samples were taken. Season of birth affected concentrations of testosterone (greater for spring-born) in intact bulls, but not luteinizing hormone (LH) or follicle stimulating hormone (FSH). The concentration of FSH increased about 30% between 4 and 32 wk, without evidence of pulsatile discharge. Basal concentration of LH was low and pulsatile discharges were infrequent at 4 or 8 wk. At 12, 16 and 20 wk, however, basal LH concentration was elevated and LH discharges were at less than 2-h intervals. Testosterone concentration did not rise until 18 to 20 wk, but then continued to rise; LH discharge was suppressed concomitantly. Bulls castrated at 16 or 20 wk had higher concentrations of LH in their blood both before and shortly after castration values for bulls, but by 21 d after castration values for bulls of all ages were similar. It was concluded that elimination of an unidentified suppressive factor allows frequent discharges of LH between 12 an 16 wk, but the testes do not respond by secreting more testosterone until 18 to 20 wk. By 24 wk, the testes are secreting more testosterone and pituitary production of LH is restored to a lower level; LH discharges decline in frequency and basal LH level declines. The high frequency discharges of LH between 12 and 20 wk are postulated to induce responsiveness of Leydig cells to LH and, thus, enable elevation of intratesticular testosterone to levels necessary for Sertoli cell differentiation and initiation of spermatogenesis.     

Comparison of luteinizing hormone, leptin and progesterone levels in the systemic circulation (Vena jugularis) and near the ovarian circulation (Vena cava caudalis) during the oestrous cycle in Mangalica and Landrace gilts

The objective of this study was to evaluate luteinizing hormone (LH) and luteal progesterone (P4) secretion in systemic blood and blood near the ovaries in Mangalica (M) and Landrace (L) gilts by implanting catheters into the Vena jugularis and the Vena cava caudalis via the Vena saphena, respectively. Furthermore, leptin was analyzed in jugular vein blood. Blood was collected twice daily from day 7 to day 19 of the oestrous cycle and frequently (10-min intervals for 6 h) on day 9, day 12 and day 15 in M (n=3) and L gilts (n=4). L gilts had congruent pulsatile LH secretion in both veins, but the LH concentrations in M were always below the assay sensitivity during the luteal phase. In both breeds, episodic P4 secretion was found in the jugular and caval veins, and both sampling site and breed had an influence on P4 secretion (P<0.05). The mean concentration of P4 was higher (P<0.01) in utero-ovarian blood (75.8+/-5.3 in M; 49.6+/-4.2 ng/ml in L) than in the periphery (31.3+/-2.0 in M; 21.2+/-1.8 ng/ml in L). M pigs had a lower number of corpora lutea (9.7+/-2.3 vs. 20.5+/-4.4), and analysis of the P4 secretion ratio per corpus luteum revealed an influence of breed (P<0.01). This ratio was significantly higher in M (3.8+/-0.3 and 8.7+/-0.7 ng/ml) compared with the L gilts (1.4+/-0.1 and 2.8+/-0.3 ng/ml) in the jugular and caval veins, respectively. Blood sampling from the Vena cava caudalis is potentially more precise than from the Vena jugularis for evaluation of ovarian P4 secretion. Both the higher P4 concentration and increased leptin secretion (11.3+/-0.6 vs. 3.0+/-0.1 ng/ml, P<0.05) and consequently the altered LH secretion pattern in the Mangalica may contribute to the lower fecundity of this breed.     

Influence of calf removal on the serum luteinizing hormone response to naloxone in the postpartum beef cow

Twelve anestrous, postpartum beef cows were used to determine the effect of calf removal on the effect of naloxone on serum luteinizing hormone (LH) concentrations. On d 1, six cows were injected iv with saline and six with 200 mg naloxone dissolved in saline. Blood samples were taken at 15-min intervals for 2 h before and 2 h after naloxone or saline administration. At the beginning of blood sampling, calves were removed from three cows in each treatment. At 48 h after calf removal (d 3), all cows were injected iv with 200 mg naloxone and blood samples were collected as on d 1. On d 1, naloxone treatment increased (P less than .01) serum LH concentrations from 1.2 +/- .3 ng/ml at time 0 to 4.3 +/- .6 ng/ml and 4.7 +/- .8 ng/ml at 15 and 30 min, respectively. Injection of saline had no effect on serum LH concentrations. Forty-eight-hour calf removal increased (P less than .01) serum LH concentrations in five of six cows (1.7 +/- .8 vs 4.4 +/- 1.2 ng/ml). Naloxone treatment failed to increase serum LH concentrations in these cows. Injection of naloxone increased (P less than .01) serum LH concentrations in the one cow that did not exhibit an LH increase after calf removal and in six cows whose calves were not removed (1.4 +/- .2 vs 4.4 +/- .5 ng/ml). The present study provides additional evidence that endogenous opioids regulate LH in the postpartum beef cow. We hypothesize that suckling stimulates an opioid inhibition of LH secretion and removal of the suckling stimulus removes the opioid inhibitory tone.     

Postpartum nutrient intake and body condition: effect on pituitary function and onset of estrus in beef cattle

From calving through first estrus, 30 Brangus females were assigned equally to one of three diets to study the effect of postpartum nutrient intake and body condition on the ability of the pituitary to release luteinizing hormone (LH) and on the postpartum interval to estrus (PPI). The postpartum diets were calculated to achieve a 1) low [90% of the National Research Council (NRC) recommendations], 2) maintenance (100% of the NRC recommendations), or 3) high (110% of the NRC recommendations) level of nutrient intake. The females were group-fed within a treatment and calves were allowed to suckle ad libitum. Cow weight, body condition score and calf weight were recorded 24 h aftercalving, d 20 postpartum and at first behavioral estrus. On d 21 postpartum, blood samples were collected via jugular cannulae at 15-min intervals for 4 h, followed by a 100-micrograms im injection of gonadotropin-releasing hormone (GnRH) and continued sampling at 15-min intervals for an additional 6 h to determine serum LH. Although there was a significant decrease in PPI with increasing levels of nutrient intake (low = 57.5 +/- 8.8 d; maintenance = 40.3 +/- 6.6 d; high = 34.7 +/- 5.1 d), there were no differences in any of the observed LH characteristics (or variables) due to treatment. There were, however, marked differences in both the PPI and LH characteristics when data were analyzed on the basis of ability to maintain body condition from calving through 20 d postpartum, regardless of calculated dietary treatments. Cows that maintained body condition (MBC) had a shorter PPI [MBC, 31.7 +/- 2.8 vs lost (LBC) 60.0 +/- 7.5 d; P less than .01], higher basal levels of endogenous LH (MBC, .83 +/- .09 vs LBC, .61 +/- .04 ng/ml; P less than .025), higher GnRH-induced peak LH concentration (MBC, 58.99 +/- 11.15 vs LBC, 38.86 +/- 8.37 ng/ml. P less than .10), higher LH levels throughout the GnRH-induced LH surge (P less than .001), and greater release curve areas for the endogenous (MBC, 124.6 +/- 13.3 vs LBC, 91.7 +/- 5.6 units; P less than .025), GnRH-induced (MBC, 4370.8 +/- 699.5 vs LBC, 3039.7 +/- 683.3 units; P less than .10) and total (MBC, 4510.7 +/- 706.7 vs LBC, 3141.9 +/- 684.7 units; P less than .10) LH release.(ABSTRACT TRUNCATED AT 400 WORDS)     

Chronic administration of recombinant ovine leptin in growing beef heifers: effects on secretion of LH, metabolic hormones, and timing of puberty

Serum concentrations of leptin increase linearly from approximately 16 wk before until the week of pubertal ovulation in beef heifers. To test the hypothesis that exogenous leptin can hasten the onset of puberty in heifers, we examined the effects of chronic administration of recombinant ovine leptin (oleptin) on timing of puberty, pulsatile and GnRH-mediated release of LH, and plasma concentrations of GH, IGF-I, and insulin. Fourteen fall-born, prepubertal heifers (Brahman x Hereford, 12 to 13 mo; 304.7+/-4.12 kg) were used. Heifers were stratified by age and BW and assigned randomly to one of two groups (seven animals per group): 1) Control; heifers received s.c. injections of saline twice daily (0700 and 1900) for 40 d; and 2) Leptin; heifers received s.c. injections of oleptin (19.2 microg/kg) twice daily at 0700 and 1900 for 40 d. Blood samples were collected at 10-min intervals for 5 h on. d 0, 5, 10, 20, 30, and 40, and twice daily, just before each treatment injection, throughout the study. On d 41, heifers received i.v. injections of GnRH at 0 (0.0011 microg/kg) and 90 min (0.22 microg/kg), with additional sampling for 5.5 h to examine releasable pools of LH. Diets promoted a gain of 0.32+/-0.09 kg/d, which did not differ between groups. Plasma concentrations of leptin increased markedly in leptin-treated heifers and were greater (P < 0.001) than controls throughout (27.8+/-0.8 vs. 4.9+/-0.12 ng/mL). None of the heifers reached puberty during the experiment, but did so within 45 d of its termination. Mean concentrations of plasma LH, GH, IGF-I, and insulin were not affected by treatment, nor was there an overall effect on the frequency of LH pulses. However, a treatment x day interaction (P = 0.02) revealed that the frequency of LH pulses (pulses/ 5 h) was greater (P = 0.03) in controls (3.6+/-0.36) than in leptin-treated heifers (1.7+/- 0.28) on d 10. Characteristics of GnRH-induced release of LH were not affected by treatment. In summary, chronically administered leptin failed to induce puberty or alter endocrine characteristics in beef heifers nearing the time of expected puberty.     

Administration of single short-acting doses of GnRH antagonist modifies pituitary and follicular function in sheep

Current study determined the effect of two different single subcutaneous doses (1.5 and 3 mg) of GnRH antagonist (GnRHa) on pituitary and follicular function in non-lactating cyclic ewes. Both doses abolished the pulsatile secretion of luteinizing hormone (LH) for at least 3 days and decreased mean LH concentration during 6 days (0.64 +/- 0.09 for control and 0.54 +/- 0.05, P < 0.005, and 0.46 +/- 0.02, P < 0.00001, for 1.5 and 3 mg, respectively). Supply of GnRHa decreased the number of large dominant follicles, so the total number of smaller follicles, 2-3 mm in size, increased in both treated groups from day 0, reaching its maximum at day 2 in ewes treated with 1.5 mg (19.83+/-1.05 versus 5.83 +/- 0.50 in the control, P < 0.005) and at day 4 in sheep treated with 3mg (18.67 +/- 0.65 versus 5.50 +/- 0.65 in the control, P < 0.0001). However, the analysis of follicular function in terms of inhibin A indicated a possible effect of the higher dose of GnRHa on follicular function. The pattern of inhibin secretion in the group treated with 3mg of GnRHa decreased after the first 48 h, reaching its lowest value on day 4.5 (182.59 +/- 3.75 to 140.28 +/- 9.91 pg/ml, P < 0.05) concentration significant lower than control sheep (171.93 +/- 6.21 pg/ml, P +/- 0.01) or treated with 1.5 mg (168.04 +/- 7.16 pg/ml, P+ /- 0.05). Hence, the use of 1.5 mg would be more suitable to induce the presence of a high number of follicles able to grow to preovulatory sizes.     

The effect of castration, estradiol and LHRH on LH secretion of lambs fed different levels of dietary energy

To examine the effect of diet on luteinizing hormone (LH) secretion, basal and luteinizing hormone releasing hormone (LHRH)-induced LH release was compared in intact or castrated-estradiol-17 beta implanted Finn-Dorset lambs. Ten to 12 wk old ram (n = 20) and ewe lambs (n = 20) were maintained under a 8L:16D photoperiod and fed for high (HG, 163 to 168 g/d) or low (LG, 76 to 103 g/d) rates of gain. Eight to 10 wk later, baseline LH concentrations were determined in blood samples collected at 20 min intervals for 7 h. The following day, lambs were given an iv injection of 5 micrograms of estradiol-17 beta followed within 4 h by LHRH (.5 or 2.5 micrograms). Baseline concentrations of LH for HG ewes were threefold greater than for LG ewes (4.2 vs 1.4 ng/ml), respectively. Time to peak response was inversely related to dietary energy level (P less than .025). Basal LH levels were similar across diets in rams. Total LH release following LHRH was dose-dependent (P less than .005). Effects of gonadal feedback were tested in a second group (n = 24) of castrated lambs. Changes in LH secretion were not different between diets within 3 to 4 wk after castration. A subcutaneous silastic implant (22 mm) of estradiol-17 beta inhibited (P less than .01) LH concentrations across diets in both ewes and rams. No differences in estradiol feedback on LH secretion (at the dose of steroid tested) were detected between HG and LG lambs. Within 8 d, however, basal LH concentrations were 60% lower (P less than .01) in HG vs LG ewes. Furthermore, peak LHRH-induced LH release was greater (P less than .025) in LG vs HG lambs of both sexes. Estradiol inhibited basal LH secretion in ewes and rams but facilitated LH release in lambs with a reduced rate of gain.     

Hormonal patterns of boars exposed to natural or supplemental lighting during pubertal development

Thirty-two crossbred boars (Hampshire X Duroc X Yorkshire) were reared under natural lighting (35 lx) or supplemental lighting (1,400 lx) beginning at 4 wk of age. Boars received supplemental lighting from six 40-W fluorescent bulbs between 0530 and 2030 in a nursery unit. From 9 to 32 wk of age, boars received either natural lighting (30 lx) or supplemental lighting (100 lx) in a growing-finishing unit. Blood samples were collected from indwelling cannulae at 20-min intervals for 6 h every 2 wk from 2.5 to 7 mo of age. Libido scores were evaluated during alternate weeks when intensive blood samples were not taken. Libido scores were not different between natural and supplemental lighting treatments (P greater than .30). However, at 122 d of age, libido scores of boars exposed to supplemental lighting tended to be higher (P = .10) than those exposed to natural lighting. Although mean serum concentrations of luteinizing hormone (LH) were higher (P less than .05) in boars at 75, 89, 103 and 131 d of age reared under supplemental lighting than boars of the same age reared under natural lighting, the number of LH secretory spikes was similar between the treatment groups (P = .39). Serum concentrations of LH decreased in both treatment groups as boars became older (P less than .05). However, the incidence of LH spikes was similar across ages and between treatment groups from 2.5 to 7 mo of age. Mean serum concentrations of follicle stimulating hormone and testosterone were similar between treatments (P greater than .75).     

Effect of photoperiod and castration on prolactin, testosterone and luteinizing hormone concentrations in male calves

After 8 wk exposure to 8 h of light per day, prolactin (PRL) averaged 18.3 ng/ml of serum in eight male calves. Four calves then received 16 h of light per day; 6 wk later (age 14 wk) PRL averaged 93.8 ng/ml of serum, whereas PRL averaged 36.9 ng/ml of serum in four calves maintained under 8 h of daily light. By wk 20, PRL was not different in calves exposed to 16 or 8 h of daily light, averaging 34.7 and 17.2 ng/ml serum. Testosterone averaged .43 ng/ml of serum at wk 8 but was greater at wk 14 in calves receiving 16 h of light daily when compared with controls receiving 8 h of light (1.92 vs. .97 ng/ml of serum). Testosterone concentrations were not different between photoperiod treatments at wk 20. Luteinizing hormone (LH) concentrations were unaffected by photoperiod. In a second experiment, four male calves were castrated at approximately 2 wk of age while four similar controls were left gonadally intact. After 8 wk exposure to 8 h of light per day, PRL averaged 12.3 ng/ml of serum in all calves. After 6 wk exposure to 16 h of light per day, PRL in serum increased in castrates to 48.0 ng/ml and in controls to 59.8 ng/ml. We conclude that serum concentrations of PRL and testosterone, but not LH, increased in bull calves receiving 16 h of light daily relative to calves receiving 8 h of light, and that the PRL response to photoperiod is independent of the testes. However, 16 h light-induced stimulation of serum concentrations of prolactin is not maintained indefinitely.     

Effect of naloxone on serum luteinizing hormone, cortisol and prolactin concentrations in anestrous beef cows

Two experiments were conducted with the opioid antagonist naloxone to determine the effect of opioid receptor blockade on hormone secretion in postpartum beef cows. In Exp. 1, nine anestrous postpartum beef cows were used to measure the effect of naloxone on serum luteinizing hormone (LH), cortisol and prolactin concentrations. Cows received either saline (n = 4) or 200 mg naloxone in saline (n = 5) iv. Blood samples were collected at 15-min intervals for 2 h before and after naloxone administration. Serum LH concentrations increased (P less than .01) in naloxone-treated cows from 1.8 +/- .04 ng/ml before treatment to 3.9 +/- .7 ng/ml and 4.2 +/- .5 ng/ml at 15 and 30 min, respectively, after naloxone administration. In contrast, LH remained unchanged in saline-treated cows (1.6 +/- .3 ng/ml). Serum cortisol and prolactin concentrations were not different between groups. In Exp. 2, 12 anestrous postpartum beef cows were used to examine the influence of days postpartum on the serum LH response to naloxone. Four cows each at 14 +/- 1.2, 28 +/- .3 and 42 +/- 1.5 d postpartum received 200 mg of naloxone in saline iv. Blood samples were taken as in the previous experiment. A second dose of naloxone was administered 2 h after the first, and blood samples were collected for a further 2 h. Serum LH concentrations increased (P less than .01) only in cows at 42 d postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)