Animal science departments of the future.

Departments of animal science were established in agricultural colleges of public universities just over 100 yr ago, shortly before the founding of today's American Society of Animal Science. These departments and colleges have been remarkably resilient, changing little structurally. Yet, the future portends significant changes in these departments and colleges in response to shifts in how public higher education is financed and how society views the roles of animals in providing food and companionship. Funding for public higher education will continue to decline as a percentage of government appropriations. Public universities will garner more funding from gifts, endowments, grants, contracts, and tuition but will be held more accountable than today by public officials. Departments of animal science will retain strong constituencies and will be major units of most agricultural colleges; however, their students and faculty will be more diverse. Departments of animal science will focus on more species of animals and on a greater role of animals in society. Disciplines of faculty members in departments of animal science will become broader, and research projects will be more complex and have longer horizons, ultimately focused more on sustainability. Departments will share more resources across state and national boundaries, and there will be less duplication of effort regionally. Departments of animal science will continue to be important academic units of universities into the 22nd century.

Role of gonadotropin-releasing hormone pulse frequency in differential regulation of gonadotropins in the gilt.

We tested the hypothesis that different GnRH pulse frequencies will affect serum LH and FSH differently. Ovariectomized gilts (n = 6), immunized against GnRH, were given 200-ng pulses of GnRH agonist (GnRH-A) every 180 min for 3 days (pretreatment), followed by GnRH-A pulses every 30, 60, or 180 min for 3 days (treatment) in a Latin rectangle design. Mean gonadotropin concentrations did not change over time when GnRH pulses were administered every 180 min. Initiation of high GnRH-A pulse frequency (30 min) caused a robust increase in serum LH to 265% of the pretreatment level (p < or = 0.007) and a more moderate increase in serum FSH to 127% of pretreatment level (p < or = 0.02). After 66 h of frequent pulsing, desensitization had occurred and serum LH concentrations were similar to pretreatment concentrations, but serum FSH had decreased to 53% of pretreatment levels (p < or = 0.0008). After 72 h of treatment, 5 micrograms GnRH-A was infused to estimate residual releasable pools of LH and FSH, and the amounts of LH and FSH released were negatively correlated with GnRH-A pulse frequency. The results of this study imply that the LH surge is terminated because the pituitary gland becomes incapable of responding to an otherwise adequate stimulus, and not because of exhaustion of releasable LH pools. Our results confirm that in the pig the response to altered GnRH-A pulse frequency differs between LH and FSH. High GnRH pulse frequency is more effective in acutely releasing LH than FSH. Low pulse frequency of GnRH supports FSH synthesis and release, but is not as effective in increasing LH concentrations, while high GnRH pulse frequency inhibits FSH synthesis and release.

Evidence for a local role of inhibin or inhibin alpha subunits in compensatory ovarian hypertrophy.

The aim of this study was to determine whether immunoneutralization of inhibin altered compensatory ovarian hypertrophy. Crossbred postpubertal gilts actively immunized with a synthetic bovine inhibin peptide fragment (bINH) conjugated to human alpha globulins (HAG, n = 4 gilts) or HAG alone (control; n = 5) were unilaterally ovariectomized at mid-cycle. After unilateral ovariectomy, the remaining ovary was removed between day 8 and day 12 of the subsequent oestrous cycle. The number of corpora lutea per ovary was determined at each ovariectomy. Blood samples were collected at frequent intervals beginning 1 h before and continuing until the first oestrus after unilateral ovariectomy, and serum concentrations of FSH, LH, progesterone and oestradiol were determined. Inhibin antibody titres were estimated from the percentage of 125I-labelled bINH bound to serum diluted 1:4000. At unilateral ovariectomy, the number of corpora lutea per ovary was similar for bINH:HAG-immunized and control gilts (8.6 +/- 0.7 versus 7.6 +/- 0.6). During the next oestrous cycle after unilateral ovariectomy, the number of corpora lutea on each remaining ovary had doubled (P < 0.05) in controls compared with the number of corpora lutea per ovary in the previous cycle. In contrast, the number of corpora lutea remained unchanged in bINH:HAG-immunized gilts. Titre of anti-inhibin antibodies in bINH:HAG-immunized gilts was 9 +/- 1% at unilateral ovariectomy compared with 0% for controls. Alterations in serum concentrations of hormones after unilateral ovariectomy did not differ between treatment groups. Compensatory ovarian hypertrophy was blocked after unilateral ovariectomy in immunized gilts independent of alterations in serum hormones, duration of oestrous cycle, or normal ovulation rate per ovary.(ABSTRACT TRUNCATED AT 250 WORDS)

Concentrations of hormones and metabolites, estimates of metabolism, performance, and reproductive performance of sows actively immunized against growth hormone-releasing factor.

Cyclic females actively immunized against growth hormone-releasing factor (GRF; n = 5) or human serum albumin (HSAi; n = 4) were used to determine the effects of reduced serum somatotropin (ST) and IGF-I on metabolism and production in gestating and lactating sows. Sows farrowed, pigs were weaned at 28 d of lactation, and sows were observed for estrus after weaning. Blood samples were collected at 15-min intervals for 5 to 6 h on d 110 of gestation and d 21 of lactation. Mean ST (nanograms/milliliter) was less (P < .05) in GRFi than in HSAi sows at d 21 of lactation, but it was similar at d 110 of gestation. Serum concentrations of IGF-I were less (P < .05) in GRFi than in HSAi sows at d 21 of lactation but not at d 110 of gestation. Serum thyroxine was greater (P < .05) in GRFi than in HSAi sows during gestation and lactation. Sows actively immunized against GRF weighed less (P < .01) and had more backfat (P < .01) at d 110 of gestation than HSAi sows; in vitro glucose oxidation and lipogenic rate of adipose tissue were greater (P < .05 for treatment x day interaction) in GRFi than in HSAi sows at d 110 of gestation. Across treatment, mammary gland oxidation of glucose and glucose clearance rates increased (P < .05), whereas adipose tissue utilization of glucose decreased (P < .05) during lactation. During lactation, GRFi sows mobilized more (P < .05) backfat than did controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Ovulatory and endocrine responses after active immunization of gilts against a synthetic fragment of bovine inhibin.

The objective of this study was to determine whether neutralizing endogenous inhibin would affect ovulation rate and serum concentrations of FSH, LH, estradiol-17 beta, and progesterone in gilts. At wk 0, during their second postpubertal estrous cycle, gilts (195 +/- 2.4 d of age) were given a primary immunization against the 1-26 gly-tyr NH-terminal amino acid sequence of bovine inhibin-alpha conjugated to human alpha globulin (INH; n = 10) or against human alpha globulin alone (control; n = 10). The primary immunization mixed with Freund's complete adjuvant contained .915 mg of the inhibin peptide. Booster immunizations in Freund's incomplete adjuvant contained .3 and .183 mg of the inhibin peptide and were given at wk 8 and 12, respectively. Free, unconjugated inhibin was given to INH gilts at 16 wk. Blood samples for determination of hormones were collected every 4 h beginning on d 15 of the first estrous cycle beyond wk 16 (first cycle) and continuing until d 5 of the second estrous cycle following wk 16 (second cycle). Ovulation rate was estimated by laparoscopy during the second cycle. Antibody titers were estimated by determining the percentage of [125I]-INH bound by serum diluted 1:4,000. The antibody titers were 17 +/- 2, 22 +/- 3, and 9 +/- 1% at wk 9, 17, and 23 for INH gilts, respectively, and 0% at all times for control gilts. Duration of three consecutive estrous cycles terminating with the first experimental cycle did not differ between treatments (INH, 20.7 +/- .3 vs control, 20.4 +/- .3 d).(ABSTRACT TRUNCATED AT 250 WORDS)

Optimizing management of natural and artificial matings in swine.

A successful mating involves the coordination of many physiological events including insemination, gamete transport and ovulation. As more basic information about these processes becomes available, it is apparent that there are opportunities for manipulating these physiological events and enhancing the reproductive success of natural and artificial matings. The primary intent of this review is to examine the effectiveness of several of these strategies, as determined by their influence on farrowing rate and litter size. It is evident that the timing, duration and pattern of ovulation in pigs are extremely variable. Thus, increasing the frequency and changing the timing of matings during oestrus has received renewed interest. In general, if a female exhibits oestrus for more than 1 day, then increasing the frequency of matings has a greater influence on reproductive performance than does altering the timing of matings. In addition, litter size is more responsive to increased mating frequencies than is farrowing rate. Increasing the number of matings per oestrus via the use of combinations of natural service and artificial insemination, compared with the use of either alone, appears to enhance reproductive performance. It has been well documented that several aspects of the mating process itself can advance the onset of ovulation and enhance sperm transport and storage in the female reproductive tract. As a result, the use of these stimuli in conjunction with natural and artificial matings provide opportunities for enhancing fecundity. Pre- and post-breeding treatments with vasectomized boars, nonviable semen, oestrogens and seminal plasma have all been reported to increase farrowing rate and litter size. With artificial insemination, additions of prostaglandins, oxytocin, oestrogens and leucocytes to semen have been reported to enhance reproductive performance, albeit with varying degrees of success. Personnel and boar needs are important components in optimizing breeding management. Estimates of these needs for artificial and natural matings are discussed.

Kinetics of follicle growth in the prepubertal gilt.

Follicular growth rates were determined by histological examination of ovaries of five prepubertal gilts following treatment with the stathmokinetic agent colchicine. One ovary from each of five gilts was removed surgically and then colchicine (n = 3) or saline (n = 2) was infused i.v. Precisely 2 h after treatment with colchicine, the remaining ovary was removed. Ovaries were processed for histological analyses and sectioned at 10 microns; every twentieth section was stained with hematoxylin and periodic acid-Schiffe's. Sections were viewed with a projection microscope and individual follicles were measured. Eight classes of follicles were established such that the number of granulosa cells per cross section doubled in each class. Diameters of follicles for each class were as follows: 1) less than 106 microns, 2) 106-148 microns, 3) 148-206 microns, 4) 206-287 microns, 5) 287-400 microns, 6) 400-657 microns, 7) 657-1480 microns, and 8) 1480-3130 microns. A layer of thecal cells was first seen in class 2 follicles, and 76% of class 3 follicles had a thecal layer. Oocyte diameter increased through the first four classes and reached a maximum diameter of approximately 110 microns. Almost all follicles greater than 400 microns had an antrum. Preantral follicles had a lower mitotic index and a higher mitotic time and class time than antral follicles. Growth rate increased with increasing size of follicles. Preantral follicles grew at a rate of 5.2 microns/day whereas antral follicles grew at 313 microns/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sexual experience, season, and mating stimuli on endocrine concentrations in the adult ram.

Two behavioral trials were conducted to determine the endocrine response of cortisol (C), luteinizing hormone (LH), testosterone (T), prolactin (PRL), and growth hormone (GH) in adult rams during exposure to estrous ewes during the breeding and nonbreeding seasons. One-half of the rams in each season were sexually experienced (SE) and the remainder were sexually inexperienced (SI). All SE rams (100%) achieved at least one ejaculation, but only 33% (summer) and 67% (fall) SI rams achieved ejaculation. In the fall, mean C, T, and GH concentrations were elevated (P less than .001) compared to values measured in the summer, whereas LH and PRL levels were higher (P less than .01) in the summer. Overall levels of C, LH, T, and PRL were higher (P less than .05) in SE rams than in SI rams. Mean GH concentration was higher (P less than .10) in SI than in SE rams during restricted and complete access to estrous ewes. In general, LH, PRL, and GH responses were similar during restricted and complete access to females for both SE and SI rams. Cortisol levels were higher (P less than .06) during periods of mating and T levels were higher (P less than .001) during periods where activity was limited to courtship behavior (nasogenital investigation). Correlations of hormones to reproductive behaviors indicated that mounting and intromission were associated with elevations in C and PRL, whereas elevated LH and T tended to be associated with courtship behaviors. Correlations between GH and behaviors were inconsistent. However, there was an increased coincidence between time of female exposure and hormonal response that occurred in the fall; brief exposure to estrous ewes resulted in increases in concentrations of all hormones examined. The most consistent response was observed in sexually experienced rams during restricted access to females during the breeding season. These results provide new information on the effects of season and level of sexual experience upon hormonal and behavioral characteristics of the ram during mating activity.

Effects of exogenous estradiol-17 beta on luteinizing hormone, progesterone, and estradiol-17 beta concentrations before and after prostaglandin F2 alpha-induced termination of pregnancy and pseudopregnancy in gilts.

This study evaluated the influence of exogenous estradiol-17 beta (E2) administration on LH concentrations and the number of animals returning to estrus after the termination of pregnancy or pseudopregnancy in gilts. Gilts were mated (pregnant; n = 11) on the 1st d of estrus or received 5 mg of estradiol valerate i.m. at d 11 to 15 after the onset of estrus (pseudopregnant; n = 9). Gilts were treated with prostaglandin F2 alpha (PGF2 alpha, 15 and 10 mg) at 12-h intervals on d 44 of pregnancy or pseudopregnancy. The day of abortion or luteolysis (progesterone less than .2 ng/mL) was considered d 0. Six pregnant and four pseudopregnant gilts received s.c. an E2 capsule (24 mg of E2) on d -20 and additional E2 capsules on d -13 and -6. The E2 capsules were removed on the day after PGF2 alpha administration. Blood samples were collected at 12-h intervals from d -21 to -3, at 6-h intervals from d -2 to 21 or the onset of estrus, and at 15-min intervals for 8 h on d -2, 1, 4, 7, 10, 14, and 18. After each 8-h sampling period, gilts were treated i.v. with GnRH at .5 micrograms/kg of BW and blood samples collected at 10-min intervals for 3 h. A greater (P less than .05) proportion of sham-treated gilts than of E2-treated gilts exhibited a preovulatory-like LH surge after abortion/luteolysis. It was evident that E2 supplementation before luteolysis reduced the ability of pregnant and pseudopregnant gilts to return to estrus.

Hourly administration of GnRH to prepubertal gilts: endocrine and ovulatory responses from 70 to 190 days of age.

This study investigated the responsiveness of the pituitary-ovarian axis of prepubertal gilts to hourly injections (i.v.) with GnRH. Six gilts each at 70, 100, 150, and 190 d of age were assigned either to treatment with GnRH or saline. Treatments were given until gilts showed estrus or for 7 d, whichever came first. Hourly pulsing with GnRH resulted in gradually increasing concentrations of estradiol-17 beta (E2), a preovulatory surge of LH, and subsequently increased progesterone (P4) concentrations. The increase in serum P4 was preceded by ovulation and corpora lutea (CL) formation in two gilts 70 d of age and all older gilts. The interval (h) from start of GnRH treatment to peak E2 (88 +/- 3), peak LH (103 +/- 3), and concentrations of P4 greater than or equal to 1 ng/mL (144 +/- 4) did not differ (P greater than .50) for 18 gilts between 100 and 190 d of age. In two ovulating, 70-d-old gilts, the interval from onset of GnRH treatment to peak E2 (171 +/- 6), peak LH (186 +/- 0), and P4 greater than or equal to 1 ng/mL (216 +/- 4) was lengthened (P less than .001). Peak concentrations of E2 (pg/mL) were higher (P less than .01) at 190 d (48 +/- 2) and 150 d (49 +/- 2) than at younger ages and lower (P less than .01) in gilts 70 d of age (31 +/- 1) than in gilts 100 d of age (41 +/- 2). Peak LH (nanograms/milliliter) was higher (P less than .01) in gilts 100 d of age (12.7 +/- 6) than in older gilts. Concentrations of P4 were similar (P greater than .20) for all ovulating gilts. The number of CL (12.7 +/- .7) did not differ (P greater than .20) for 18 gilts 100 d of age or older but was higher (P less than .01) than that (4.5 +/- 1.1) for two gilts 70 d of age. Corresponding endocrine responses or ovulations were not observed in four 70-d-old gilts treated with GnRH or in gilts given saline. These findings indicate that the functional integration of the pituitary-ovarian axis is completed between 70 and 100 d of age. Hourly treatment with GnRH is an adequate stimulus to induce ovulation in prepubertal gilts as early as 70 d of age. Also, the number of follicles reaching ovulatory competency was similar (P greater than .20) in gilts between 100 and 190 d of age, when GnRH was given on a BW basis.

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.

Impairment of follicular development by intra-ovarian infusion of gonadotrophin-releasing hormone antiserum in prepubertal pigs.

Antiserum against gonadotrophin-releasing hormone (GnRH) was infused into one ovary in 4 prepubertal gilts and control porcine serum was infused into one ovary in 4 other gilts. Ovaries were infused for 156 h, after which infused and non-infused ovaries were removed surgically and processed for histology. Infusion of GnRH antibodies did not alter (P greater than 0.10) concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH) or oestradiol-17 beta, and GnRH titres in peripheral circulation were low, averaging 1:15. Weights of ovaries not infused were similar (P greater than 0.10) between treatment groups. There were fewer (P less than 0.05) follicles greater than 0.5 mm in diameter in the ovaries infused with GnRH antiserum than in the others, but there were no differences (P greater than 0.10) between treatment groups in the number of follicles less than 0.5 mm in diameter. Infusion of GnRH antibodies increased (P less than 0.05) the incidence of atresia in follicles with greater than 4 layers of granulosa cells compared with the other treatment groups. These results provide evidence that a peptide binding to the GnRH antibodies is involved directly in ovarian follicular development.

Effects of pretreatment with adrenocorticotropin on endocrine and behavioral responses of bulls to sexual activity.

Peripheral concentrations of cortisol, growth hormone and testosterone were determined in two experiments which examined the endocrine and behavioral responses of sexually mature Angus bulls to an estrous female (Experiment 1) and to female exposure 5 hours following an adrenocorticotropin (ACTH) injection (Experiment 2). Sexual activity of bulls in Experiment 1 significantly increased levels of cortisol when compared with concentrations before exposure to a female. Administration of ACTH in Experiment 2 consistently elevated levels of cortisol by 30-fold (P<0.01) when compared with pre-ACTH concentrations. This heightened level of cortisol persisted throughout the period of exposure to an estrous cow, although a gradual decline in cortisol concentrations occurred over time (P<0.05). In Experiment 1, growth hormone profiles tended to increase in response to sexual activity (P<0.10), whereas in Experiment 2, growth hormone increased in response to ACTH administration (P<0.01) and to female exposure (P<0.01). Concentrations of testosterone were unaffected (P>0.10) by mating activity in Experiment 1. In Experiment 2, acute suppression (P<0.01) in testosterone concentrations 5 hours after ACTH administration coincided with the exposure period to the estrous female. Frequencies of mounting behavious (penis extension, mounting, intromission and ejaculation) exhibited by ACTH-treated bulls were significantly lower compared with the frequencies two days earlier. Exogenous ACTH administration suppressed reproductive behaviors of bulls and altered secretion of cortisol, growth hormone and testosterone. Furthermore, these data provide evidence that specific mating behaviors of the bull can be influenced by circulating steroids.

Roles of estradiol and gonadotropin-releasing hormone in controlling negative and positive feedback associated with the luteinizing hormone surge in ovariectomized pigs.

Ovariectomized gilts (n = 63) were given estradiol benzoate (estradiol), antiserum to neutralize endogenous GnRH, and pulses of a GnRH agonist (GnRH-A) to stimulate release of LH. GnRH-A was given as 200-ng pulses hourly from 0 to 54 h and as 100- or 200-ng pulses every 30 or 60 min from 54 to 96 h after estradiol. Estradiol alone suppressed LH from 6 to 54 h and elicited an LH surge that peaked at 72 h. When GnRH-A was given every 30-60 min from 0 to 96 h, estradiol suppressed LH for 6-12 h, but then LH returned to pre-estradiol concentrations. When pulses of GnRH-A were given only between 54 and 96 h after estradiol, the surge of LH was related positively to dose and frequency of GnRH-A. We conclude that 1) estrogen acts at the hypothalamus to inhibit release of GnRH for 54 h and then causes a synchronous release of GnRH; 2) estrogen acts at the pituitary to block its response to GnRH for 6-12 h and enhances the accumulation of releasable LH; and 3) magnitude of the LH surge is dependent on the amount of GnRH stimulation.

Cortisol, growth hormone, and testosterone concentrations during mating behavior in the bull and boar.

Two experiments were conducted to evaluate peripheral concentrations of cortisol (C), growth hormone (GH), and testosterone (T) in bulls and boars during mating and to correlate mating behaviors with endocrine secretion in the presence of an estrous female. In Exp. 1, six sexually inexperienced mature bulls were bled every 15 min for 2 h before and 2 h after a 30-min exposure to a single, restrained, estrous cow; sampling occurred every 5 min during exposure. In Exp. 2, six sexually experienced boars were bled similarly before and after exposure to a sow and every 5 min during a 15-min exposure to a freely moving, estrous sow. Behavioral events recorded during exposure to a female included the following: flehmen responses (bulls only), mounts, penis extensions, intromissions, ejaculations, and time to first mount and first ejaculation. Of the six bulls, four completed at least one service (intromission + ejaculation), and three of six mounted the estrous cow eight or more times. Completion of one or more services resulted in significant elevations in serum C and GH concentrations, but not T concentrations, during the exposure period. Bulls mounting eight or more times also experienced significant elevations in C concentrations during exposure. Three of six boars completed at least one service. Servicing and mounting the sow fewer than five times were both associated with significant elevations in serum C concentrations. Serum concentrations of T were also elevated as a result of exposure to an estrous sow. Collectively, these data support the suggestion that specific events during natural mating activity can alter endocrine secretions of C and GH in bulls and C and T in boars.

Passive immunization of the pig against gonadotropin releasing hormone during the follicular phase of the estrous cycle.

Three experiments were conducted to determine the effects of passively immunizing pigs against gonadotropin releasing hormone (GnRH) during the follicular phase of the estrous cycle. In Experiment 1, sows were given GnRH antibodies at weaning and they lacked estrogen secretion during the five days immediately after weaning and had delayed returns to estrus. In Experiment 2, gilts passively immunized against GnRH on Day 16 or 17 of the estrous cycle (Day 0 = first day of estrus) had lower (P<0.03) concentrations of estradiol-17beta than control gilts, and they did not exhibited estrus at the expected time (Days 18 to 22). When observed three weeks after passive immunization, control gilts had corpora lutea present on their ovaries, whereas GnRH-immunized gilts had follicles and no corpora lutea. The amount of GnRH antiserum given did not alter (P<0.05) serum concentrations of LH or pulsatile release of LH in sows and gilts. In Experiment 3, prepuberal gilts were given 1,000 IU PMSG at 0 h and GnRH antiserum at 72 and 120 h. This treatment lowered the preovulatory surge of LH and FSH, but it did not alter serum estradiol-17beta concentrations, the proportion of pigs exhibiting estrus, or the ovulation rate. These results indicate that passive immunization of pigs against GnRH before initiation of or during the early part of the follicular phase of the estrous cycle retards follicular development, whereas administration of GnRH antibodies during the latter stages of follicular development does not have an affect. Since the concentration of antibodies was not high enough to alter basal or pulsatile LH secretion, the mechanism of action of the GnRH antiserum may involve a direct ovarian action.

Effect of feeding thyrotropin-releasing hormone to lactating sows.

Two experiments were conducted to assess the effects of feeding thyrotropin-releasing hormone (TRH) during lactation on sows. In Exp. 1, sows were fed 0, 1, 10, 100 or 1,000 mg TRH on d 10.8 +/- .4 (mean +/- SE) after parturition. Blood samples were taken from sows every 30 min from -2 h to 8 h and at 10, 12 and 18 h from feeding. Consumption of 100 or 1,000 mg TRH increased mean serum concentrations of thyroxine (T4; P less than .001), 1,000 mg TRH increased growth hormone (GH; P less than .06) and 100 or 1,000 mg TRH increased prolactin (PRL; P less than .01), but insulin (INS; P greater than .10) was unaffected by TRH. Serum concentrations of T4 were elevated within 2 to 4 h after feeding TRH and remained elevated for 12 to 18 h. Concentrations of GH and PRL began to increase immediately after feeding 100 or 1,000 mg TRH and remained elevated for 6 and 8 h, respectively. In Exp. 2, sows were fed 0 or 200 mg TRH from d 111 of gestation to weaning at 27.1 +/- .3 d of lactation. Consumption of TRH elevated concentrations of T4 at all stages of lactation and increased respiration rate on d 10 and d 20, heart rate on d 20, and milk production on d 20 of lactation. Consumption of TRH did not influence number of pigs born, number born alive, survival rate during lactation, sow body weight, heartgirth, backfat depth, feed disappearance, or milk production on d 10 of lactation. Piglets nursing sows fed TRH were similar in weight to piglets nursing sows not fed TRH on d 0 and 5 of lactation, but they were heavier on d 10 (P less than .07), 15 (P less than .001), 20 (P less than .001) and 27 (P less than .0001). Sows fed TRH took longer (P less than .001) to return to estrus after weaning than control sows. Results indicated that feeding TRH elevated T4, GH and PRL and that feeding TRH for the duration of lactation increased milk production on d 20 of lactation and increased weaning weights, but it delayed estrus after weaning.

The effect of human growth hormone-releasing factor or porcine somatotropin on serum hormones and metabolites, growth performance and carcass traits in swine.

Forty barrows (77.9 +/- 5.5 kg BW) were allotted to one of five treatment groups to examine the effects of various doses of human growth hormone-releasing factor (1-44)NH2 (hGRF) or porcine somatotropin (pST) administered twice daily on serum hormones and metabolites, performance and carcass traits. Barrows were injected s.c. with either a placebo, 10 micrograms hGRF.kg BW-1.12 h-1, 20 micrograms hGRF.kg BW-1.12 h-1, 20 micrograms pST.kg BW-1.12 h-1 or 40 micrograms pST.kg BW-1.12 h-1 for a 36-d growth trial. Blood samples were collected from 13 barrows at intervals for 360 min after injection on d 21. Compared with the placebo, 10 micrograms hGRF.kg-1.12 h-1 increased (P less than .01) serum pST and insulin and decreased (P less than .001) urea N. Injecting 20 micrograms hGRF/kg.12 h-1 elevated (P less than .001) serum pST, insulin and insulin-like growth factor-I (IGF-I) but lowered (P less than .001) urea N. Exogenous pST increased (P less than .001) serum pST, insulin, IGF-I and glucose but decreased (P less than .001) urea N. Growth rate tended to increase, and feed intake and feed/gain decreased, in a dose-related manner in response to hGRF. Also, pigs receiving 10 or 20 micrograms hGRF.kg-1.12 h-1 had reduced (P less than .1) backfat and increased (P less than .1) loineye area and percentage lean in the ham compared with pigs receiving the placebo. At equal doses, pST elicited more dramatic improvements in performance and carcass criteria than did hGRF.(ABSTRACT TRUNCATED AT 250 WORDS)

Opioid control of growth hormone in the suckled sow is primarily mediated through growth hormone releasing factor.

Endogenous opioid peptides mediate the effect of suckling on LH and PRL in the domestic pig. However, the role of opioids in modulating GH during lactation in swine is not known. Primiparous sows that had been immunized against GRF(1-29) conjugated to human serum albumin (GRF-HSA, n = 5) or HSA (n = 4) were used to determine changes in GH after naloxone. Treatments were imposed in all sows on day 21 of lactation when antibody titers were 9100 +/- 1629. All sows received (i.v.) naloxone (0.25 mg/kg) or saline (0.0125 ml/kg) at 15 min intervals for 165 min. Active immunization against GRF-HSA during lactation decreased (P less than 0.05) mean concentration (4.8 +/- 0.2 vs 2.6 +/- 0.1 ng/ml) and frequency (1.5 +/- 0.3 vs 0.4 +/- 0.2 peaks/4 hr). Concentrations of LH and PRL were similar in GRF-HSA and HSA immunized sows. Naloxone suppressed (P less than 0.05) GH in all sows. In HSA sows, naloxone abolished episodic release of GH and decreased average, but not basal, concentrations of GH. In sows immunized against GRF-HSA, naloxone decreased (P less than 0.05) average and basal GH but failed to decrease frequency of GH release. Naloxone failed to alter frequency of LH release. Concentrations of PRL decreased (P less than 0.05) after naloxone in all sows. In conclusion, immunization against GRF-HSA blocked most of the effect of lactation on GH. Blocking opioid receptors with naloxone decreased GH and PRL in all sows. In contrast to previous findings naloxone had no effect on LH. Opioids alter concentrations of GH through a GRF dependent and GRF independent pathway.

Ontogeny of the gonadal receptor for luteinizing hormone in the pig.

Homogenates of porcine ovaries and testes collected between 70 d post coitum and 42 d post partum were incubated with radiolabelled human chorionic gonadotropin (hCG) to determine the presence and relative amounts of luteinizing hormone/human chorionic gonadotropin (LH/hCG) receptors. Specific binding of (125)I-hCG to ovaries and testes occurred at all stages of fetal and postnatal development. Ovarian tissue possessed relatively low affinity, high capacity LH/hCG binding sites that were most numerous at Day 80 of gestation and decreased thereafter. In contrast, high affinity, low capacity LH/hCG binding sites were found in the testes. In males, the total number of LH/hCG binding sites remained stable until near term and then increased with age, but the number of sites per gram of testicular tissue did not change (P>0.05). In summary, differential binding of LH/hCG in gonadal tissue occurred in male and female piglets during pre- and post-natal periods, and this binding reflected the known differential pattern of development of the male and female gonad.