N-methyl-d,l-aspartate stimulates growth hormone and prolactin but inhibits luteinizing hormone secretion in the pig.

The effects of n-methyl-d,l-aspartate (NMA), a neuroexcitatory amino acid agonist, on luteinizing hormone (LH), prolactin (PRL) and growth hormone (GH) secretion in gilts treated with ovarian steroids was studied. Mature gilts which had displayed one or more estrous cycles of 18 to 22 d were ovariectomized and assigned to one of three treatments administered i.m.: corn oil vehicle (V; n = 6); 10 micrograms estradiol-17 b/kg BW given 33 hr before NMA (E; n = 6); .85 mg progesterone/kg BW given twice daily for 6 d prior to NMA (P4; n = 6). Blood was collected via jugular cannulae every 15 min for 6 hr. Pigs received 10 mg NMA/kg BW i.v. 2 hr after blood collection began and a combined synthetic [Ala15]-h GH releasing factor (1-29)-NH2 (GRF; 1 micrograms/kg BW) and gonadotropin releasing hormone (GnRH; .2 micrograms/kg BW) challenge given i.v. 3 hr after NMA. NMA did not alter LH secretion in E gilts. However, NMA decreased (P < .02) serum LH concentrations in V and P4 gilts. Serum LH concentrations increased (P < .01) after GnRH in all gilts. NMA did not alter PRL secretion in P4 pigs, but increased (P < .01) serum PRL concentrations in V and E animals. Treatment with NMA increased (P < .01) GH secretion in all animals while the GRF challenge increased (P < .01) serum GH concentrations in all animals except in V treated pigs. NMA increased (P < .05) cortisol secretion in all treatment groups. These results indicate that NMA inhibits LH secretion and is a secretagogue of PRL, GH and cortisol secretion with ovarian steroids modulating the LH and PRL response to NMA.     

Opioid inhibition stimulates luteinizing hormone and prolactin secretion in the gilt

Ten gilts on day 6·11 of the estrous cycle (onset of estrus = day 0) were given 115 mg of naloxone (NAL), an opioid antagonist, in saline i.v. (n = 5) or saline Lv. (n = 5). Jugular blood was collected at 15 min intervals for 2 hr before and 4 hr after treatment. Serum LH concentrations were 0.4 ± 0.1 ng/ml before NAL treatment, increased (P<.01) to 4.3 ± 0.7 ng/ml at 15 min following NAL treatment and returned to control concentrations by 75 minutes. Serum PRL concentrations were 5.0 ± 0.1 ng/ml before NAL treatment, increased (P<.05) to 14.8 ± 2.9 ng/ml at 30 min following NAL treatment and returned to control concentrations by 120 minutes. Serum LH and PRL concentrations were 0.5 ± 0.1 ng/ml and 5.2 ± 0.4 ng/ml, respectively, at 15 min following saline treatment and remained unchanged throughout the blood sampling period. Four of the 5 NAL treated gilts responded with an increase in both serum LH and PRL concentrations. The mean of serum progesterone concentrations, quantitated in samples taken every 2 hr, were similar for controls (22.7 ± 1.8 ng/ml) and NAL (26.5 ± 1.4 ng/ml) treated gilts. The gilt which failed to respond to NAL had nondetectable concentrations of serum progesterone and was excluded from analysis. These data indicate that the opioids modulate LH and PRL secretion during the luteal phase of the estrous cycle.     

Recommendations for clinical GnRH challenge testing of stallions

Eight mature light-breed stallions with normal testes size, sperm output and semen quality were used to evaluate response to 3 GnRH challenge regimens in the summer in southeast Texas. Gonadotropin releasing hormone (50 μg) was administered intravenously once to each of eight stallions after three days of sexual rest (50 μg GnRH-1X). The same stallions were administered either 5μg GnRH intravenously once hourly for three injections (5 μg GnRH-3X) and 15μg GnRH intravenously once (15μg GnRH-1X) one and two weeks later. Blood samples were collected prior to and at intervals after GnRH administration. Plasma was immediately separated from blood samples and was frozen until assayed for LH, FSH, estradiol and testosterone concentrations. Percentage changes in hormone concentrations from pre-treatment values (baseline) were analyzed by paired studient'st-test to detect significant rises in hormone concentrations. Group mean percentage changes in hormone concentrations were analyzed by analysis of variance to compare responses among treatments. A computerized peak-detection algorithm (PC Pulsar) was used to detect peaks in LH and testosterone concentrations following 5 μg GnRH-3X and 15 μg GnRH-1X treatment.No differences (P>0.10) were detected in percentage change from baseline concentration for LH, FSH, or testosterone at one or two hours after administration of any of the three regimens of GnRH. When more frequent sampling intervals were analyzed for 5 μg GnRH-3X or 15 μg GnRH-1X treatments, no differences were detected in percentage change from baseline concentration for any hormone at 15, 30 or 60 minutes. Thereafter, percentage changes in concentrations of LH and FSH remained increased for 5μg GnRH-3X compared to 15 μg GnRH-1X treated stallions (P<0.05). Percentage changes in concentrations of testosterone were increased for 5μg GnRH-3X compared to 15 μg GnRH-1X treated stallions from 180–300 min (P<0.05), while no differences (P>0.10) were detected between 5 μg GnRH-3X and 15 μg GnRH-1X treated stallions for changes in concentrations of estradiol throughout the experiment.For 15 μg GnRH-1X treated stallions, maximum concentrations of LH in PC Pulsar-detected peaks occurred most commonly at 15 to 30 minutes (7/8 treatment periods) after GnRH injection. Maximum concentrations of testosterone in PC Pulsar-detected peaks occurred most commonly at 60–120 min (7/8 treatment periods) after GnRH injection.A protocol of blood sampling prior to, and 15, 30, 60 and 120 minutes after, intravenous administration of small doses of GnRH would be practical for challenge testing of stallions during the breeding season. In order to reduce cost of hormone assays, we suggest assay of the pre-challenge blood sample (baseline) could include LH, FSH, testosterone and estradiol concentrations (to assess overall hypothalamic-pituitary-testicularfunction), while only LH and testosterone concentrations need be determined after GnRH administration (to assess pituitary and testicular responsiveness). Assay for LH could be done on only the 15 and 30 minute post-GnRH samples, and assay for testosterone could be done on only the 60 and 120 minute post-GnRH samples. Failure to achieve approximately a 50% increase in LH concentration by 30 minutes after GnRH administration, and/or failure to achieve approximately a 100% increase in testosterone concentration by two hours after GnRH administration, could be further pursued either by treatment with increasing dosages of GnRH, or repeated administration of GnRH at hourly intervals, as has been suggested by other workers.     

Pituitary responsiveness to GnRH, hypothalamic content of GnRH and pituitary LH and FSH concentrations immediately preceding puberty in gilts

To determine whether pituitary concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH) or hypothalamic content of gonadotropin releasing hormone (GnRH) change before puberty, 40 prepubertal gilts averaging 7 mo of age were slaughtered before or on the second, third or fourth day after relocation and boar exposure. Some gilts responded to relocation and boar exposure as indicated by swollen vulvae, turgid uteri and enlarged ovarian follicles at the time of slaughter. Pituitary concentrations of LH and FSH and hypothalamic content of GnRH were similar between gilts that responded to relocation and boar exposure and gilts that did not respond. In addition, boar exposure and relocation had no effect on pituitary concentrations of LH and FSH or on hypothalamic content of GnRH. To determine whether pituitary responsiveness to GnRH changes before puberty, a third experiment was conducted in which 72 gilts were injected with 400 micrograms of GnRH either before or on the second, third or fourth day after relocation and boar exposure. In gilts that subsequently responded (i.e., ovulated) as a result of relocation and boar exposure, pituitary responsiveness to GnRH was reduced as compared with gilts that failed to ovulate after relocation and boar exposure. Peak concentrations of serum LH after GnRH injection were 4.6 +/- 1.3 vs 9.8 +/- .8 ng/ml for responders vs nonresponders. Peak serum FSH after GnRH injection was also lower for responders than for nonresponders (29.5 +/- 4.2 vs 41.2 +/- 2.4 ng/ml). When compared with controls, relocation and boar exposure did not significantly affect GnRH-induced release of LH and FSH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Elicitation of release of luteinizing hormone by N-methyl-d,l-aspartic acid during three paradigms of suppressed secretion of luteinizing hormone in the female pig.

Two experiments were conducted to determine the minimal effective dose during lactation and site of action of N-methyl-d,l-aspartic acid (NMA) for elicitation of release of luteinizing hormone (LH) in female pigs. In the first experiment, three doses of NMA were given to lactating primiparous sows in which endogenous LH was suppressed by suckling of litters. In the second experiment, ovariectomized gilts were pretreated with estradiol benzoate or porcine antisera against GnRH to suppress LH and then given NMA to determine if it elicited secretion of LH directly at the anterior pituitary or through release of GnRH. In experiment 1, 3 lactating sows (17 +/- 1.5 d postpartum) were each given three doses of NMA (1.5, 3.0 and 5.0 mg/kg body weight [BW]; IV) on 3 consecutive days in a Latin Square design. Blood samples were collected every 10 min from -1 to 1 hr from injection of NMA. NMA at 1.5 and 3.0 mg/kg did not affect (p greater than .5) secretion of LH; however, 5 mg NMA/kg elicited a 114% increase (p less than .001) in circulating levels of LH during 1 hr after treatment. In experiment 2, 8 ovariectomized gilts were given either estradiol benzoate (EB; 10 micrograms/kg BW; IM n = 4) to suppress release of GnRH or porcine antiserum against GnRH (GnRH-Ab; titer 1:8,000; 1 ml/kg BW; IV; n = 4) to neutralize endogenous GnRH. Gilts infused with GnRH-Ab were given a second dose of antiserum 24 hr after the first. Gilts were then given NMA (10 mg/kg BW; IV) 33 hr after EB or initial GnRH-Ab. Blood samples were drawn every 6 hr from -12 to 24 hr from EB or GnRH-Ab treatments, and every 10 min from -2 to 2 hr from NMA. Serum LH declined (p less than .001) after EB (from 1.87 +/- .2 ng/ml at 12 hr before EB to 0.46 +/- .02 ng/ml during 24 hr after EB) and GnRH-Ab (from 1.97 +/- .1 to 0.59 +/- .02 ng/ml). In gilts treated with EB, the area under the curve (AUC) for the LH response (ng.ml-1.min) 1 hr after NMA (38.7 +/- 3) was significantly greater (p less than .01) than the 1 hr prior to NMA (21.3 +/- 1.5). Treatment with NMA had no effect (p greater than .5) on secretion of LH in gilts infused with GnRH-Ab.(ABSTRACT TRUNCATED AT 400 WORDS)     

Opioid modulation of gonadotropin releasing hormone release from the hypothalamic preoptic area in the pig

Two experiments (Exp) were conducted to examine in vitro the release of gonadotropin releasing hormone (GnRH) from the hypothalamus after treatment with naloxone (NAL) or morphine (MOR). In Exp 1, hypothalamic-preoptic area (HYP-POA) collected from 3 market weight gilts at sacrifice and sagitally halved were perifused for 90 min prior to a 10 min pulse of morphine (MOR; 4.5 × 10⁻⁶ M) followed by NAL (3.1 × 10⁻⁵ M) during the last 5 min of MOR (MOR + NAL; N=3). The other half of the explants (n=3) were exposed to NAL for 5 min. Fragments were exposed to KCl (60 mM) at 175 min to assess residual GnRH releasability. In Exp 2, nine gilts were ovariectomized and received either oil vehicle im (V; n=3); 10 μg estradiol-17β/kg BW im 42 hr before sacrifice (E; n=3); .85 mg progesterone/kg BW im twice daily for 6 d prior to sacrifice (P₄; n=3). Blood was collected to assess pituitary sensitivity to GnRH (.2 μg/kg BW) on the day prior to sacrifice. On the day of sacrifice HYP-POA explants were collected and treated as described in Exp 1 except tissue received only NAL. In Exp 1, NAL increased (P<.05) GnRH release. This response to NAL was attenuated (P<.05) by coadministration of MOR. Cumulative GnRH release after NAL was greater (P<.05) than after MOR + NAL. All tissues responded similarly to KCl with an increase (P<.05) in GnRH release. In Exp 2, pretreatment luteinizing hormone (LH) concentrations were lower (P<.05) in E gilts compared to V and P₄ animals with P₄ being lower (P<.05) than V gilts. LH response to GnRH was lower (P<.05) in E pigs than in V and P₄ animals, while the responses was similar between V and P₄ gilts. NAL increased GnRH release in all explants, whereas, KCl increased GnRH release in 6 of 9 explants. These results indicate that endogenous opioid peptides may modulate in vitro GnRH release from the hypothalamus in the gilt.     

Influence of the duration of photoperiod on growth,testicular characteristics and endocrine function of boars

Crossbred boars were used to evaluate the influence of exposure to 8 or 16 hr of light daily from 75 to 175 days of age on growth rate, testicular characteristics and endocrine function. At 160 days of age, concentrations of testosterone in serum (P<.10), the areas under plotted 12 hr testosterone profiles (P<.10) and the number (P<.05) and magnitude (P<.10) of testosterone secretory spikes were increased in boars exposed to 16 hr of light compared to boars in 8 hr light, but concentrations of LH in serum were similar in boars exposed to both treatments. Treatment with GnRH resulted in similar concentrations of LH in serum for both groups of boars. Testosterone in serum after GnRH-mediated LH release was greater at .5 (P<.05) and 1.0 (P<.10) hr following GnRH in boars exposed to 16 hr of light compared to boars at 8 hr, but concentrations of testosterone were similar for both treatments from 1.5 to 4.0 hr after GnRH. Growth rate and testicular and epididymal weights and sperm reserves at 175 days of age were not significantly altered by duration of photoperiod. Boars exposed to 8 hr of light had more hair per unit area than boars exposed to 16 hr of light. We conclude that exposure of prepubertal boars to longer daily photoperiods results in increased concentrations of testosterone in serum at 160 days of age.     

Effects of various mating stimuli on pituitary release of luteinizing hormone in the gilt

Twenty-four nulliparous crossbred gilts approximately 9 months of age were assigned to either a naturally mated (NM), artificially inseminated (Al) or non-mated control group (C). All gilts were fitted with indwelling cephalic cannulas for collection of blood samples for subsequent hormonal analyses every 10 min for the first 24 hr of the periestrous period. Plasma luteinizing hormone (LH) concentrations were not affected by type of mating. The mean duration of the LH surge for Al group was less than the C or NM groups (44.5 vs 67 and 87 hr (P<.05)). Mean maximal LH concentrations for the Al and NM groups occurred prior to the control group (P> 05). Area under the LH release curve and number of episodic surges were not different for the three treatments. Length of standing estrus and exposure time to back pressure were not different among treatment groups.The results suggest that stimulation of the pelvic region during either natural mating or artificial insemination did not enhance release of LH. Mated gilts did exhibit different secretory patterns of LH release than non-mated gilts.     

Effects of sodium pentobarbital on release of gonadotropins in ewes immediately after ovariectomy and after treatment with gonadotropin-releas ing hormone

Two experiments were conducted with ewes 9 to 11 days after estrus to determine whether the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are controlled differentially. In experiment 1, gonadotropin-releasing hormone (GnRH) was injected (100 (μg/ewe) at time = 0 min into ewes in four treatment groups. The treatment groups (9 ewes/group) were: 1) periodic iv sodium pentobarbital (NaPen) vehicle from 0 min; 2) periodic iv NaPen from 0 min; 3) vehicle iv for 120 min then iv NaPen from 120 min; 4) vehicle iv for 150 min then iv NaPen from 150 min. A surgical plane of anesthesia was maintained from the initiation of NaPen injection until the experiment ended. Jugular blood was sampled at 30-min intervals from ?30 to + 210 min for LH and FSH assays, and profiles of hormone concentrations were compared by time-trend analyses. GnRH released LH (P<.001) and FSH (P<.001), but NaPen did not affect the profiles of hormone concentrations; this indicated that NaPen did not reduce the ability of the pituitary to secrete gonadotropins in response to GnRH. Experiment 2 was a 2x2 factorial with ovariectomy (time = 0 hr) and NaPen as the main effects. One group of ovariectomized (n = 6) and one group of sham ovariectomized (n = 6) ewes were anesthetized only during surgery, while a group of ovariectomized (n = 7) and a group of sham ovariectomized (n = 6) ewes were kept at a surgical plane of anesthesia until 10 hr after surgery. Patterns of LH and FSH were compared in jugular blood collected hourly from 0 hr until 10 hr after surgery and in samples collected at 24 hr intervals from -24 to +72 hr of surgery. After ovariectomy, LH increased (P<.001) hourly and daily, but anesthesia suppressed (hourly, <.001 and daily, P<.005) these increases, which resulted in an interaction (hourly, P<.001 and daily, P<.01) of ovariectomy and anesthesia. FSH after ovariectomy increased hourly and daily (hourly, P<.02 and daily, P<.001), but the effect of anesthesia and interaction of ovariectomy and anesthesia were not significant. Because NaPen did not alter secretion of LH or FSH after exogenous GnRH in experiment 1 while it blocked the postovariectomy increase in LH but not FSH in experiment 2, we concluded that the postovariectomy increase in LH resulted from increased hypothalamic secretion of GnRH. The mechanisms responsible for the postovariectomy increase in FSH secretion are not identical to those for LH. The mechanisms that control the postovariectomy secretion of FSH might involve factors that are not suppressible by NaPen or, alternatively, the differences in LH and FSH release after ovariectomy might reflect the removal of ovarian factors that suppress FSH but not LH secretion in intact ewes.     

Luteinizing hormone (LH) response to different doses of synthetic gonadotropin releasing hormone (GnRH) in prepubertal gilts

The object of this investigation was to study luteinizing hormone (LH) response to different doses of synthetic gonadotropin-releasing hormone (GnRH) in prepubertal gilts. Four crossbred prepubertal gilts, 128–134 days old and body weight 57–63 kg, were used in this study. Four doses, 0. 5, 25 and 125 μg, of GnRH were administered via a jugular vein catheter in a latin square design. Each treatment consisted of 3 injections at 90 min intervals. Frequent blood samples were taken during a period of 90 min before up to 90 min after treatment. Total LH responses were measured from post-treatment samples as the area under the curve above base level obtained from pre-treatment samples. A positive relationship between GnRH dose and LH release was obtained in all gilts, except for 1 treatment given to a gilt with high plasma level of oestradiol-17β on the day of treatment. This study has demonstrated the responsiveness of the pituitary gland by LH release to different doses of GnRH in 4.5-month-old prepubertal gilts.     

The effect of pulsatile gonadotropin-releasing hormone and estradiol administration on luteinizing hormone and follicle-stimulating hormone concentrations in pituitary stalk-sectioned ovariectomized pony mares

Hourly pulses of gonadotropin-releasing hormone (GnRH) or bi-daily injections of estradiol (E2) can increase luteinizing hormone (LH) secretion in ovariectomized, anestrous pony mares. However, the site (pituitary versus hypothalamus) of positive feedback of estradiol on gonadotropin secretion has not been described in mares. Thus, one of our objectives involved investigating the feedback of estradiol on the pituitary. The second objective consisted of determining if hourly pulses of GnRH could re-establish physiological LH and FSH concentrations after pituitary stalk-section (PSS), and the third objective was to describe the declining time trends of LH and FSH secretion after PSS. During summer months, ovariectomized pony mares were divided into three groups: Group 1 (control, n = 2), Group 2 (pulsatile GnRH (25 μg/hr), n = 3), and Group 3 (estradiol (5 mg/12 hr), n = 3). All mares were stalk-sectioned and treatment begun immediately after stalk-section. Blood samples were collected every 30 min for 8 h on the day before surgery (DO) and 5 d post surgery (D5) to facilitate the comparison of gonadotropin levels before and after pituitary stalk-section. Additionally, jugular blood samples were collected every 12 hr beginning the evening of surgery, allowing for evaluation of the gonadotropin secretory time trends over the 10 d of treatment. On Day 10, animals were euthanized to confirm pituitary stalk-section and to submit tissue for messenger RNA analysis (parallel study). Plasma samples were assayed for LH and FSH by RIA. Mean LH secretion decreased from Day 0 to Day 5 in Groups 1 and 3, whereas LH secretion tended (P < 0.08) to decrease in Group 2 mares. On Day 5, LH was higher (P < 0.01) in Group 2 (17.26 ± 3.68 ng/ml; LSMEANS ± SEM), than either Group 1 (2.65 ± 4.64 ng/ml) or group 3 (4.28 ± 3.68 ng/ml). Group 1 did not differ from Group 3 on Day 5 (P < 0.40). Similarly, mean FSH levels decreased in all groups after surgery, yet Group 2 mares had significantly (P < 0.001) higher FSH concentrations (17.66 ± 1.53 ng/ml) than Group 1 or Group 3 (8.34 ± 1.84 and 7.69 ± 1. 63 ng/ml, respectively). Regression analysis of bi-daily LH and FSH levels indicated that the time trends were not parallel. These findings indicate: 1) Pituitary stalk-section lowered LH and FSH to undetectable levels within 5 d after surgery, 2) pulsatile administration of GnRH (25 μg/hr) maintained LH and FSH secretion, although concentrations tended to be lower than on Day 0, and 3) E2 did not stimulate LH or FSH secretion.     

Luteinizing hormone secretion in hypophysial stalk-transected gilts given hydrocortisone acetate and pulsatile gonadotropin-releasing hormone.

The site within the hypothalamic-pituitary axis at which cortisol acts to inhibit luteinizing hormone (LH) secretion was investigated in female pigs. Six ovariectomized, hypophysial stalk-transected (HST) gilts were given 1 microgram pulses of gonadotropin releasing-hormone (GnRH) iv every 45 min from day 0 to 12. On days 6-12, each of 3 gilts received either hydrocortisone acetate (HCA; 3.2 mg/kg body weight) or oil vehicle im at 12-hr intervals. Four ovariectomized, pituitary stalk-intact gilts served as controls and received HCA and pulses of 3.5% sodium citrate. Jugular blood was sampled daily and every 15 min for 5 hr on days 5 and 12. Treatment with HCA decreased serum LH concentrations and LH pulse frequency in stalk-intact animals. In contrast, serum LH concentrations, as well as the frequency and amplitude of LH pulses, were unaffected by HCA in HST gilts and were similar to those observed in oil-treated HST gilts. We suggest that chronically elevated concentrations of circulating cortisol inhibit LH secretion in pigs by acting at the level of the hypothalamus.     

Ovulation and embryonic survival in pubertal gilts treated with gonadotropin releasing hormone

An experiment was conducted to evaluate the effect of exogenous gonadotropin releasing hormone (GnRH) on ovulation and embryonic survival in pubertal gilts. Gilts were assigned in replicates to a control (n = 10) and treatment (n = 10) group. Treatment consisted of an iv injection of 200 micrograms of GnRH immediately after initial mating on the first day of detected estrus. Control gilts were similarly injected with physiological saline. Blood samples were collected from the anterior vena cava immediately prior to injection, thereafter at 15-min intervals for 90 min, and subsequently, before slaughter on d 30 of gestation. Serum samples were analyzed for luteinizing hormone (LH) and progesterone by radioimmunoassay. Treatment with GnRH increased the quantity of LH released (P less than .05), with highest serum concentrations (ng/ml, means +/- SE) of gonadotropin in treated gilts (17.3 +/- 3.5) occurring at 75 min post-injection. In control gilts, serum concentrations of LH were not affected by injection of saline. Mean number of ovulations in treated gilts was also greater (P less than .05) than that of control animals (14.5 +/- .7 vs 12.1 +/- .6). However, treatment with GnRH did not enhance the number of attached conceptuses (normal and degenerating) present (treated, 10.9 +/- .9 vs control, 10.5 +/- .7) nor the percentage of viable fetuses (treated, 74.7 +/- 6.9 vs control, 83.5 +/- 5.0%) on d 30 of gestation. Although GnRH increased ovulation rate, mean weight of corpora lutea of treated and control gilts did not differ (402.8 +/- 16.3 vs 389.5 +/- 11.3 mg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of pulsatile injection of GnRH into 6- to 14-wk-old Holstein bulls

With the goal of hastening puberty, we evaluated the effects of dose of gonadotropin releasing hormone (GnRH) during pulsatile injection on luteinizing hormone (LH) secretion in bulls 6, 10 or 14 wk old, and of pulsatile administration of GnRH every 2 h to bulls from 6 to 12 wk of age on reproductive development. Based on response to the last three of 12 bihourly injections of 20, 200 or 2,000 ng GnRH/kg, only the two higher doses of GnRH induced secretion of LH at 6 wk. At all ages, 200 ng GnRH/kg induced maximal discharges of LH. Based on comparisons between seven treated bulls and their identical twins, bihourly injections of GnRH starting on d 42 elicited discharge of LH for less than or equal to 4 d in progeny of one sire and greater than 28 d but less than 42 d in progeny of another sire. After 14 d of treatment, both elicited and spontaneous discharges of LH were smaller in all treated bulls. Within 2 d after cessation of GnRH injections on d 84, LH discharges were similar in frequency and amplitude in treated and control twins. Testicular and body growth were similar in treated and control bulls, but puberty was delayed (P less than .05) in bulls in which exogenous GnRH suppressed endogenous discharges of LH.     

Treatment with Gonadotropin Releasing-Hormone in Prepubertal Gilts at Two Different Ages

To study the effect of GnRH in prepubertal gilts, seven crossbred gilts were treated with saline solution and 250 fig GnRH. In connection with saline and GnRH treatments blood was sampled every 15 min for 4 h, thereafter every 30 min for 2 h and every 60 min for 3 h, and finally every 3 h for 6 days. The ovaries were inspected by laparo-scopy just before and 6 days after GnRH treatment. The first GnRH treatment was undertaken when the gilts had a mean age of 141 days and mean body weight of 66 kg. One gilt was in prooestrus at this treatment. In the other 6 gilts the mean LH level was around 0.5 μg/l during a 4 h period after the saline injection. After the GnRH treatment a LH peak was seen with a mean duration of 4 h and a mean maximum level of 9.2 ± 2.07 μg/1. None of the gilts ovulated or showed oestrus within a week after GnRH treatment, which was confirmed by laparoscopy. The seventh gilt which was in prooestrus had high levels of oestradiol-17β (> 40 pmol/1) at GnRH treatment and no LH peak was seen during a 4 h period after treatment.Two gilts which had not shown oestrus at an age of 173 days and a mean body weight of 93 kg were treated a second time with 250 μg GnRH. The LH peak had a duration of 4 h and a mean maximum level of 5.3 ± 3.04 μg/l. Neither of these 2 gilts showed oestrus or ovulated within a week after GnRH injection. It was concluded that a single injection of GnRH results in a LH peak but is not enough to stimulate ovulation or oestrus in prepubertal gilts at a mean age either of 141 or 173 days.Key words: GnRH-treatment, prepubertal gilts, LH, oestradiol-17β     

Endogenous opioid suppression of release of luteinizing hormone during suckling in postpartum anestrous beef cows

Beef cows were used to determine if suckling influences release of LH via endogenous opioids at 28 +/- 4 d after parturition. Cows of similar weight and body condition (6.8 +/- .1, 1 = emaciated, 9 = obese) were assigned randomly to five groups (n = 6 to 7): 1) control-suckled/saline (suckled 15 min every 6 hr for 48 hr); 2) control-suckled/naloxone; 3) calf-removal/saline (calf removal for 52 hr); 4) calf-removal/naloxone; and 5) control-suckled/GnRH (Gonadotropin-Releasing Hormone). At 0 hr, saline was administered to all cows. This treatment was continued at 6 hr intervals for 24 hr. Either naloxone (0.5 mg/kg), GnRH (40 ng/kg) or saline was administered to cows in their respective groups every 6 hr during the ensuing 24-hr period in calf-removal groups, or immediately preceding each suckling episode in the control-suckled groups. Blood samples for analysis of luteinizing hormone (LH) were collected at 15-min intervals for 1 hr prior to and 3 hr after treatment at 0, 24, 36 and 48 hr. Cows were observed for estrus twice daily. All cows in the control-suckled/GnRH group released LH (P less than .05) in response to exogenous GnRH, indicating the presence of releasable quantities of the gonadotropin. Mean concentrations of LH were not effected (P greater than .05) by the control-suckled regime. However, calf-removal alone, or in combination with naloxone, increased (P less than .05) mean concentrations of LH by 48 hr.(ABSTRACT TRUNCATED AT 250 WORDS)     

Genetic parameter estimates for reproductive traits of male and female littermate swine

Reproductive traits of purebred and crossbred pigs produced in a four-breed diallel mating system using the Duroc, Landrace, Spotted and Yorkshire breeds were collected for five consecutive farrowing seasons (two farrowing seasons/year) beginning in fall 1976. Paternal half-sib heritabilities and genetic correlations for testicular traits (120 boars from 36 sires), serum testosterone (TE) and luteinizing hormone (LH) concentrations before and after treatment with gonadotropin releasing hormone (GnRH; 131 boars from 37 sires) and breeding performance traits (151 boars from 38 sires) were estimated. Heritability estimates were generally small to moderate except for sperm/gram testis (SGT), LH concentrations before (LHO) and at 3 h (LH3) after treatment with GnRH (.73 +/- .48, .61 +/- .46 and 1.19 +/- .45, respectively). A large positive genetic correlation was found for LHO with LH3 (.94 +/- .39), while a negative relationship existed for LH3 with TE concentrations at 3 h after GnRH injection. The genetic correlation between a boar's average first service conception rate and average conception rate also was significant (.82 +/- .54). Genetic correlations among littermate traits would suggest that selection for decreased age at puberty in gilts could cause an increase in LH concentrations in boar offspring, before and after GnRH injection, and may also have adverse effects on their ability to settle females. Selection for increased weight at puberty of gilts could cause TE concentrations of boar offspring to increase while having little effect on their breeding performance.     

N-methyl-d,l-aspartate modulation of pituitary hormone secretion in the pig: Role of opioid peptides

Sixteen ovariectomized (OVX) mature gilts, averaging 139.6 ± 3.1 kg body weight (BW) were assigned randomly to receive either progesterone (P, 0.85 mg/kg BW, n=8) or corn oil vehicle (OIL, n=8) injections im twice daily for 10 d. On the day of experiment, all gilts received either the EAA agonist, N-methyl-d,l-aspartate (NMA; 10 mg/kg BW, iv) alone or NMA plus the EOP antagonist, naloxone (NAL, 1 mg/kg BW, iv), resulting in the following groups of 4 gilts each: OIL-NMA, OIL-NMA-NAL, P-NMA and P-NMA-NAL. Blood samples were collected via jugular cannula every 15 min for 6 hr. All pigs received NMA 5 min following pretreatment with either 0.9% saline or NAL 2 hr after blood collection began and a GnRH challenge 3 hr after NMA. Administration of NMA suppressed (P<0.03) LH secretion in OIL-NMA gilts and treatment with NAL failed to reverse the suppressive effect of NMA on LH secretion in OIL-NMA-NAL gilts. Similar to OIL-NMA gilts, NMA decreased (P<0.03) mean serum LH concentrations in P-NMA gilts. However, in P-NMA-NAL gilts, serum LH concentrations were not changed following treatment. All gilts responded to GnRH with increased (P<0.01) LH secretion. Additionally, administration of NMA increased (P<0.01) growth hormone (GH) and prolactin (PRL) secretion in both OIL-NMA and P-NMA gilts, but this increase in GH and PRL secretion was attenuated (P<0.01) by pretreatment with NAL in OIL-NMA-NAL and P-NMA-NAL gilts. Serum cortisol concentrations increased (P<0.01) in all gilts and the magnitude of the cortisol response was not different among groups. In summary, results of the present study confirmed previous findings that NMA suppresses LH secretion in both oil- and P-treated OVX gilts, but we failed to provide definitive evidence that EOP are involved in the NMA-induced suppression of LH secretion. However, NMA may, in part, activate the EOP system which in turn increased GH and PRL secretion in the gilt.     

The influence of exogenous pituitary growth hormone on the ovulatory response to PMSG and hCG and the LH response to estradiol benzoate in prepubertal gilts

Two experiments were performed to examine the influence of exogenous growth hormone on the reproductive axis in gilts. Experiment one employed 26 Yorkshire × Landrace prepubertal gilts, which were selected at 150 d and 86.5 ± 1.5 kg bodyweight (BW) and assigned equally to two treatments. Gilts received injections of either porcine growth hormone at 90 μg/kg BW, or vehicle buffer, from 150 to 159 d. At 154 d gilts received 500 IU PMSG, followed 96 hr later by 250 IU hCG. Gilts were slaughtered at 163 days and their ovaries recovered to determine ovulatory status. In each treatment, gilts failed to show any ovarian response to PMSG/hCG. All remaining control gilts ovulated and their ovaries appeared morphologically normal. In gilts receiving exogenous growth hormone, fewer ovaries (4/11, P<.01) appeared morphologically normal. The ovaries of all other growth hormone injected gilts had very large (12–25 mm) non-luteinized follicles. In experiment two, 20 prepubertal Yorkshire × Landrace gilts were selected at 138 days and 85 kg BW. These gilts received injections of growth hormone at 90 μg/kg BW (n=9) or vehicle (n=11) from 138 to 147 days. At 143 days, all gilts were given an injection of estradiol benzoate (EB) at 15 μg/kg BW. Blood samples were taken at the time of EB injection, at 24 and 36 hr and then at 6 hr intervals until 78 hr. All samples were assayed for serum LH concentrations. The EB induced LH peak height was lower (P<.04) in gilts receiving exogenous growth hormone than in controls. The results presented indicate that the daily injection of growth hormone at 90 μg/kg BW reduced the estradiol-induced release of LH in addition to reducing the number of corpora lutea in gonadotrophin stimulated gilts.     

Serum profiles of progesterone, LH, FSH and prolactin immediately preceding induced puberty in gilts

Two experiments were conducted to determine if the secretory patterns of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) and serum concentrations of progesterone change immediately preceding induced puberty in gilts. To help predict when prepubertal gilts would attain puberty, gilts were induced into puberty by relocation from confinement housing to an outdoor lot and exposure to mature boars. In Exp. 1, 17 prepubertal gilts were bled on two successive days from 0800 to 1200 h before relocation and boar exposure and until the second day of estrus or for 8 d in gilts that failed to exhibit estrus. Blood samples were collected from indwelling cannulas at 20-min intervals for 4 h. In Exp. 2, blood samples were collected from 20 prepubertal gilts at 20-min intervals from 0800 to 1200 h and from 2000 to 2400 h until the second day of estrus or for 6 d if the gilt failed to exhibit estrus. In each experiment, 11 gilts exhibited pubertal estrus 3 to 6 d after relocation and boar exposure. When the frequency of LH spikes in each gilt was normalized to the day of her preovulatory surge of LH (d 0), a decline in the frequency of LH secretory spikes was observed as gilts approached puberty. However, neither the average magnitude of LH spikes nor mean LH concentrations were different among these days. Mean serum concentrations, frequency of spikes or average magnitude of secretory spikes of FSH or PRL did not change on the days preceding the preovulatory peak of LH.(ABSTRACT TRUNCATED AT 250 WORDS)