Central administration of corticotrophin-releasing factor in the sheep: effects on secretion of gonadotrophins, prolactin and cortisol
- 1 January 1990
- journal article
- research article
- Published by Bioscientifica in Journal of Endocrinology
- Vol. 124 (1) , 117-125
- https://doi.org/10.1677/joe.0.1240117
Abstract
Stress interferes with the normal secretion of LH and FSH from the anterior pituitary gland and therefore exerts a deleterious effect on reproductive function. Evidence suggests that the stress-induced disruption of gonadal function is due to a central action of corticotrophin-releasing factor (CRF) to inhibit the release of LHRH into the hypophysial-portal circulation. The following studies were undertaken to investigate further the role of CRF in regulating gonadotrophin release in the sheep and to determine whether central administration of this peptide can alter the secretion of other hormones (e.g. prolactin and cortisol) known to be released under conditions of stress. In contrast to other species, injection of CRF into the third ventricle of the sheep brain caused a dose-related stimulation of LH secretion. The pulse frequency and mean levels of LH were increased significantly following central administration of CRF. In contrast to this effect, central administration of CRF did not alter the plasma concentration of FSH but caused a marked and dose-related stimulation of prolactin and cortisol secretion. The stimulatory effect of CRF on prolactin secretion was reversed by i.v. administration of the opioid antagonist naloxone, suggesting that endogenous opioid peptides mediate the central effect of CRF on the release of prolactin, but not cortisol. In conclusion, these data demonstrate that administration of CRF causes a dose-related stimulation of LH and prolactin release from the anterior pituitary gland and cortisol from the adrenal gland. In the case of prolactin, endogenous opioid peptides are likely to mediate this response. The observations concerning LH are the opposite of those reported for the rat and the monkey where CRF caused a prolonged inhibition of gonadotrophin secretion. This suggests that a species difference may exist or, alternatively, the stimulatory effect of CRF on LH secretion in the sheep may be similar to the increase in LH secretion reported in rats and monkeys subjected to short-term handling or restraint stress. Journal of Endocrinology (1990) 124, 117–125This publication has 41 references indexed in Scilit:
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