Development of Pig Oocytes Activated by Stimulation of an Exogenous G Protein-Coupled Receptor1

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Abstract
It is generally accepted that corticotropin-releasing hormone (CRH) is the central mediator of stress-activated changes in the pituitary-adrenal axis because it results in the release of ACTH and ultimately increases the systemic levels of cortisol. And, because in some situations CRH also inhibits the hypothalamic release of GnRH, it has been presumed that it plays the central role in stress-related reduction in pituitary-gonadal function as well. We previously have shown that 6 h of restraint stress in intact female rhesus macaques suppresses plasma levels of LH in the follicular but not the luteal phase of the menstrual cycle and that this effect lasts beyond the period of restraint. Since CRH inhibits both the GnRH pulse generator and LH release in ovariectomized macaques and is generally thought to be the central mediator of stress-induced inhibition of gonadotropin release, we investigated the influence of CRH administration on LH in undisturbed intact female rhesus macaques. Blood samples were collected at 15-min intervals for 15 h from a remote site from female macaques in both the follicular and luteal phase. During this time, each animal received a 4-h infusion of CRH (100-micrograms bolus followed by 100 micrograms/h for 4 h) through an indwelling jugular catheter. Blood samples were collected for an additional 8 h after cessation of the CRH infusion. Cortisol levels were significantly elevated during and after the CRH infusion and were comparable to levels observed in animals that experienced restraint. However, CRH did not suppress LH levels in either the follicular or the luteal phase.(ABSTRACT TRUNCATED AT 250 WORDS)