Secretion of gonadotropins and estimated releasable pools of gonadotropin-releasing hormone and gonadotropins during establishment of suckling-induced inhibition of gonadotropin secretion in the sow.

Two experiments were conducted to evaluate relationships between changes in hypothalamic GnRH, pituitary and serum gonadotropins, and ovarian function during the first week postpartum in lactating multiparous sows. In experiment 1, our hypothesis was that sows would have active LH secretion immediately after parturition and that suckling would inhibit LH concentrations within the first 3 days postpartum. Sows were killed at Day 1 (n = 5) or Day 7 (n = 5) of lactation, and blood samples were taken every 6 h from 48 h before parturition until 24 h (Day 1 sows) or 156 h (Day 7 sows) after parturition. Preoptic area (POA), medial basal hypothalamus (MBH), stalk median eminence (SME), anterior pituitary (AP), and ovaries were collected at slaughter. On Day 1, sows had fewer (p < 0.05) small follicles (< 4 mm diameter), but more (p < 0.05) medium (4-6 mm) and large (> 6 mm) follicles, than sows on Day 7 (20 +/- 2, 6.5 +/- 1.1, 2.5 +/- 0.7 vs. 26.3 +/- 3, 0, and 0, respectively). Serum LH and FSH decreased (p < 0.04) during the period from 24 to 48 h postpartum and remained low through Day 7. GnRH concentrations in POA, MBH, and SME and the proportion of residual GnRH released in vitro in response to K+ did not differ between Day 1 and 7. Weights of AP were not different, but pituitary concentrations (microgram/mg) of LH and FSH increased (p < 0.05) from Day 1 to 7 (LH: 0.27 +/- 0.03 vs. 0.44 +/- 0.01; FSH: 2.6 +/- 0.07 vs. 7.8 +/- 0.8, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Agonist-induced release of gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone and their associations with basal secretion of luteinizing hormone and follicle-stimulating hormone throughout lactation in sows.

Our working hypothesis was that the normal increase in basal secretion of LH and FSH during lactation in sows is paralleled by an increase in readily releasable pools of GnRH, LH, and FSH. Sows fitted with indwelling catheters and nursing 9-11 piglets were sampled on Days 1, 7, 14, and 21 (primiparous sows; n = 10; experiment 1) or Days 7 and 21 (multiparous sows; n = 10; experiment 2) of lactation. On each day, blood was collected at 10-min intervals for 2 h before one member of a pair of sows was infused (i.v.) with saline (n = 5) and the other with the neuroexcitatory amino acid N-methyl-DL-aspartic acid (NMA; 10 mg/kg b.w.) to measure readily releasable GnRH as estimated by LH release. Two hours later, each sow that had received saline was given GnRH (100 micrograms, i.v.) for estimation of releasable pools of pituitary LH and FSH. Responses to NMA and GnRH were estimated by area under the curve (ng.ml-1.min) of serum LH profiles for 1 h (NMA group) or 2 h (GnRH group) after treatment. Basal LH secretion in primiparous sows decreased from Day 1 to Day 7 and then returned to Day 1 values by Day 21. Similarly, in multiparous sows, basal LH was lower on Day 7 than on Day 21. Basal FSH secretion increased linearly as lactation progressed in primiparous and multiparous sows.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship of secretion of GnRH in vitro to changes in pituitary concentrations of LH and FSH and serum concentrations of LH during lactation in sows.

The objectives of this study were (1) to determine whether release of GnRH in vitro was related to concentrations of LH and FSH in serum and pituitaries and to oestradiol in serum of sows at mid- or late lactation, and (2) to determine whether weaning at mid-lactation changes concentrations of these hormones from values expected at mid-lactation to values expected at late lactation. Multiparous crossbred sows were killed on day 14 (n = 5) or day 28 (n = 5) of lactation or on day 14 post partum after litters had been weaned on day 10 (n = 5). Blood samples were taken every 6 h for 4 days before sows were killed, and the preoptic suprachiasmatic area, medial basal hypothalamus, stalk median eminence, anterior pituitary and ovaries were collected at slaughter. Sows killed on day 14 after having their litters weaned on day 10 had more (P < 0.01) preovulatory follicles (> 6 mm in diameter) than lactating sows killed on day 14 or 28 (7.0 +/- 1.2 versus 0.2 +/- 0.1 and 1.5 +/- 0.8, respectively). Concentrations of LH, FSH and oestradiol in serum during 90 h before slaughter were greater (P < 0.05) in weaned sows and lactating sows killed on day 28 than in lactating sows killed on day 14 (LH: 0.72 +/- 0.3 and 0.68 +/- 0.3 versus 0.45 +/- 0.2 ng ml-1; FSH: 39.3 +/- 2.7 and 57.3 +/- 4.0 versus 28.8 +/- 1.6 ng ml-1; oestradiol: 10.9 +/- 1.6 and 5.6 +/- 0.7 versus 2.7 +/- 0.2 pg ml-1, respectively).(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)

Influence of stage of lactation, exogenous luteinizing hormone-releasing hormone, and suckling on estrus, positive feedback of luteinizing hormone, and ovulation in sows treated with estrogen.

The overall objective of this study was to investigate the LH response and occurrence of estrus and ovulation in sows treated with estradiol benzoate (EB) at mid- (d 14) or late (d 28) lactation. Experiment 1 tested the hypothesis that hourly pulses of LHRH given to sows treated with EB would cause a greater proportion to exhibit LH surges. Sows (n = 32) at mid- or late lactation were given (i.m.) corn oil (CO) or EB (10 micrograms/kg BW) at 0 h and no pulses or hourly pulses (100 ng/pulse) of the LHRH agonist des-Gly10,[D-ALA6]-LHRH ethylamide (LHRH-A) from 54 to 96 h, the anticipated period of positive feedback of LH. Blood samples for determination of estradiol-17 beta (E2) and LH were collected every 6 h from -12 to 120 h from sows treated with EB. Estrus was checked daily with a mature boar, and ovulation was assessed by measuring progesterone in blood 1 wk after estrus induced by EB or 2 wk after weaning at 34 +/- 1.4 d postpartum. Lactational estrus occurred in 0 of 16 and 15 of 16 sows given CO and EB, respectively; however, no sow ovulated in response to EB. Concentrations of LH were lower (P < .01) during mid- than during late lactation, and LHRH-A pulses had no effect on secretion of LH and E2. The LH concentrations during the pretreatment (-12 to 0 h), negative feedback (6 to 54 h), and positive feedback (60 to 96 h) periods at mid-lactation (.32 +/- .03, .22 +/- .01, and .54 +/- .08 ng/mL, respectively) differed (P < .01) from values at late lactation (.80 +/- .06, .49 +/- .02, and 1.47 +/- .17, respectively). Preovulatory-like surges of LH occurred in one of eight (peak 2.1 ng/mL) and seven of eight (peak 2.9 +/- 1 ng/mL) sows given EB at mid- and late lactation, respectively. Experiment 2 tested the hypothesis that the hypothalamus and pituitary of sows weaned 96 h before they were given EB would show a greater responsiveness than those weaned and given EB simultaneously. Sows (n = 16) at mid- or late lactation were treated with EB (10 micrograms/kg BW; i.m.), and one-half of the sows were suckled until the moment of EB treatment, whereas the other half had their litters weaned 96 h before treatment with EB.(ABSTRACT TRUNCATED AT 400 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)