Document Detail


Regulation and action of gonadotrophins in pigs.
MedLine Citation:
PMID:  2192037     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 that develop to ovulatory 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 stalk-transected pigs when pulses of GnRH are given simultaneously with the PMSG. 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 GnRH-like 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 the central 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.(ABSTRACT TRUNCATED AT 400 WORDS)
Authors:
K L Esbenshade; A J Ziecik; J H Britt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of reproduction and fertility. Supplement     Volume:  40     ISSN:  0449-3087     ISO Abbreviation:  J. Reprod. Fertil. Suppl.     Publication Date:  1990  
Date Detail:
Created Date:  1990-07-26     Completed Date:  1990-07-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0225652     Medline TA:  J Reprod Fertil Suppl     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  19-32     Citation Subset:  IM    
Affiliation:
Department of Animal Science, North Carolina State University, Raleigh 27695-7621.
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MeSH Terms
Descriptor/Qualifier:
Animals
Gonadotropins, Pituitary / physiology*
Swine / physiology*
Chemical
Reg. No./Substance:
0/Gonadotropins, Pituitary

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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