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)

Sexually mature gilts were actively immunized against gonadotropin-releasing hormone (GnRH) by conjugating GnRH to bovine serum albumin, emulsifying the conjugate in Freund's adjuvant, and giving the emulsion as a primary immunization at Week 0 and as booster immunizations at Weeks 10 and 14. Antibody titers were evident by 2 wk after primary immunization and increased markedly in response to booster immunizations. Active immunization against GnRH caused gonadotropins to decline to nondetectable levels, gonadal steroids to decline to basal levels, and the gilts to become acyclic. Prolactin concentrations in peripheral circulation were unaffected by immunization against GnRH. The endocrine status of the hypothalamic-pituitary-ovarian axis was examined by giving GnRH and two agonists to GnRH and by ovariectomy. An i.v. injection of 100 micrograms GnRH caused release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in control animals, but not in gilts immunized against GnRH. In contrast, administration of 5 micrograms D-(Ala6, des-Gly-NH2(10] ethylamide or 5 micrograms D-(Ser-t-But6, des-Gly-NH2(10] ethylamide resulted in immediate release of LH and FSH in both control and GnRH-immunized gilts. Circulating concentrations of LH and FSH increased after ovariectomy in the controls, but remained at nondetectable levels in gilts immunized against GnRH. Prolactin concentrations did not change in response to ovariectomy. We conclude that cyclic gilts can be actively immunized against GnRH and that this causes cessation of estrous cycles and inhibits secretion of LH, FSH, and gonadal steroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal changes during the follicular phase of gilts exhibiting their first estrus were examined in response to either relocation and boar exposure or treatment with pregnant mare serum gonadotropin (PMSG). In the first experiment, blood was collected from nine gilts from 6 d before to 6 d after the onset of first estrus. Mean estradiol-17 beta (E2 beta) concentrations increased from d -6 to a peak on d -2 of 20 pg/ml (d 0 = of estrus) and then declined gradually over the next 6 d until basal levels (2.4 pg/ml) were reached. Mean concentrations of luteinizing hormone (LH) fluctuated between .5 to 1 ng/ml before d 1.5 and after d 1.5, with the ovulatory surge occurring on either d -1 or d 0 and averaging 6.2 ng/ml. Progesterone (P) concentrations were less than .3 ng/ml until formation of corpora lutea, while concentrations of glucocorticoids (CORT) ranged from 7.4 to 24.5 ng/ml. In Exp. 2, blood was collected every 6 h from d -2 to d 14 from eight gilts that were exposed to boars on d 0. Four of the gilts exhibited estrus and had a hormonal profile similar to that of gilts in Exp. 1. Concentrations of E2 beta were elevated in two gilts after exposure to a boar, but concentrations of LH were not altered. The remaining two gilts had basal concentrations of E2 beta and LH throughout the blood sampling period. In Exp. 3, blood was sampled from five gilts twice daily for 8 d following the administration of 1,000 IU PMSG. Estrus was exhibited by all gilts on the fifth day after PMSG. Circulating concentrations of total estrogens peaked on -1 while concentrations of LH peaked on d 0. Concentrations of P were low until after estrus and CORT levels displayed a diurnal pattern throughout. The results indicate that the hormonal profiles during the pubertal follicular phase of gilts induced by relocation and boar exposure or PMSG are similar. Furthermore, no changes were observed in P concentrations immediately before or during the pubertal follicular phase, suggesting that progesterone priming may not be prerequisite to puberty in gilts.

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.

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