Ovarian function after autotransplantation of the adenohypophysis in the pig

Kraeling, Robert R.

doi:10.31274/rtd-180813-916

Cited by 4 publications

(3 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accepted June 1, 1987 puberal (Baker and Coggins, 1968) and anes o trous (Dziuk and Dhindsa, 1969) gilts and in anestrous lactating (Hausler et al, 1980;Hodson et al, 1981) and weaned (Dial et al, 1984) sows. Follicular growth also has been stimulated in prepuberal gilts by giving porcine pituitary extract (Kraeling, 1970), and frequent pulses of gonadotropin releasing hormone (GnRH; Carpenter and Anderson, 1985 ;Lutz et al, 1985), in postpartum sows by a crude follicle stimulating hormone (FSH) preparation (Peters et al, 1968(Peters et al, , 1969, and in anestrous lactating and weaned sows by pulsatile administration of GnRH (Cox and Britt, 1982;Armstrong and Britt, 1985).…”

Section: Introductionmentioning

confidence: 99%

Ovarian Response to Pregnant Mare Serum Gonadotropin and Porcine Pituitary Extract in Gilts Actively Immunized against Gonadotropin Releasing Hormone

1987

Journal of Animal Science

View full text Add to dashboard Cite

Two experiments were conducted to determine the effect of exogenous gonadotropins on follicular development in gilts actively immunized against gonadotropin releasing hormone (GnRH). Four gilts, which had become acyclic after immunization against GnRH, and four control gilts were given 1,000 IU pregnant mare serum gonadotropin (PMSG), while four additional control gilts were given saline. Control animals were prepuberal crossbred gilts averaging 100 kg body weight. Control gilts given saline had ovaries containing antral follicles (4 to 6 mm in diameter). Control gilts given PMSG exhibited estrus and their ovaries contained corpora hemorrhagica and corpora lutea. PMSG failed to stimulate follicular growth in gilts immunized against GnRH, and ovaries contained regressed corpora albicantia and small antral follicles (less than 1 mm in diameter). Concentrations of luteinizing hormone (LH) and estradiol-17 beta (E2) were non-detectable in gilts immunized against GnRH and given PMSG. In the second experiment, five gilts actively immunized against GnRH were given increasing doses of PMSG every third day until unilateral ovariectomy on d 50. PMSG failed to stimulate follicular growth, and concentrations of follicle stimulating hormone (FSH), E2 and LH were not detectable. Six weeks later, gilts were given a booster immunization and then were given 112 micrograms LH and 15 micrograms FSH intravenously every 6 h for 9 d. The remaining ovary was removed on d 10. Although LH and FSH concentrations were elevated, administration of gonadotropins did not stimulate follicular growth or increase E2 concentrations. These results indicate that neither PMSG or exogenous LH and FSH can induce E2 synthesis or sustain follicular development in gilts actively immunized against GnRH.

show abstract

Section: Introductionmentioning

confidence: 99%

Ovarian Response to Pregnant Mare Serum Gonadotropin and Porcine Pituitary Extract in Gilts Actively Immunized against Gonadotropin Releasing Hormone

1987

Journal of Animal Science

View full text Add to dashboard Cite

show abstract

“…An aqueous extract of lyophilized pituitaries, prepared as described previously, given to hypophysectomized gilts or gilts actively immunized against Gn RH has produced conflicting results. Kraeling (1970) reported that daily intramuscular injections of a pituitary extract induced follicular growth and ovulation, but Esbenshade (1987) gave a pituitary extract intravenously every 6 h for 9 days and did not observe a stimulation of follicular growth or an increase in peripheral concentration of oestradiol. Anderson et at (1967) gave desiccated pig anterior pituitary to mated, hypophysial stalk-transectioned gins for at least 20 days and this treatment maintained corpora lutea, progesterone production and pregnancy, but they reported that only atretic follicles were observed in the ovaries at the conclusion of treatment.…”

Section: Use Of Purified Gonadotrophinsmentioning

confidence: 99%

“…These animals therefore could not respond to treatment with exogenous gonadotrophin, but could respond if gonadotrophins in the circulation were maintained by treatment with GnRH. Evidence to refute this notion includes the induction of follicular growth in hypophysectomised gilts with a pituitary extract (Kraeling, 1970) and the observation that acyclic gilts immunized against GnRH eventually resume normal reproductive cycles and reproductive function (K. L. Esbenshade, unpublished data).…”

Section: Use Of Purified Gonadotrophinsmentioning

confidence: 99%

Regulation and action of gonadotrophinsin pigs

Esbenshade¹,

Ziecikt²,

Britt³

2020

Proc

View full text Add to dashboard Cite

Gonadotrophins, synthesized and secreted from the basophils of the adenohypophysis, bind to various target cells and elicit a wide variety of responses. Specific receptors for gonadotrophins have been found on plasma membranes of thecal, granulosa, luteal, endometrial and myometrial cells in the female and on Leydig and Sertoli cells in the Male. Gonadotrophins exert their effects through various intracellular second messengers and control biosynthetic pathways of steroid production in responsive cells. Gonadotrophins stimulate growth and development of antral follicles in the female. PMSG, FSH, or hourly pulses of GnRH, LH or a combination of LH and FSH induce follicular growth and development in prepubertal gilts and lactating and(or)anoestrous sows. The number of follicles Ilia t develop to ovula tory size in response to PMSG and FSH is dose-dependent, but pulsatile treatment with GnRH or gonadotrophins results in an ovulation rate similar to that observed during spontaneous follicular development. Endocrine changes resulting from treatments that induce follicular growth and development are similar to those observed during the follicular phase of the oestrous cycle. Hypophysectomy, hypophysial-stalk transection, active and passive immunization against GnRH, and active immunization against LH impair reproduction by interfering with normal follicular development in the female. Gonadotrophins, administered to gilts as repeated injections of whole pituitary extract or as pulses of GnRH agonist, do not stimulate follicular growth in gilts actively immunized against GnRH. Similarly, PMSG is ineffective in inducing follicular growth and development in gilts actively immunized against GnRH and after hypophysectomy or hypophysial-stalk transection. In contrast, PMSG is effective for inducing follicular development in hypophysial stalktransected pigs when pulses of GnRH are given simultaneously with the PM SG. These results suggest that agents in addition to the gonadotrophins are required for the full complement of follicular growth, recruitment and development. Insulin, growth factors and steroids modify the response of cells to the gonadotrophins and may mediate these effects. Other possibilities include substances released from the pituitary gland or GnRHlike peptide(s) produced by the ovary that act as autocrine or paracrine regulators of follicular development. Gonadotrophins stimulate testicular function in the male. Active immunization of mature boars against GnRH or LH results in testicular atrophy, depressed steroidogenic and spermatogenic functions and impaired libido. Treatment of boars immunized against GnRH with hCG restores steroidogenic function of the testes as evidenced by testosterone production. Gonadotrophins also exert an influence in thecentral nervous system. Administration of hCG intramuscularly or intracranially blocks the oestrogen-induced preovulatory LH surge in ovariectomized pigs via a short loop feedback control mechanism. Exogenous

show abstract