A reduction in the availability of oxidizable metabolic fuels inhibits reproduction. When ovariectomized, steroid-primed hamsters are food deprived for 48 hours, estrous behavior is suppressed. However, the specific neuroendocrine alterations that mediate the suppression or restoration of estrous behavior are unknown. In the following set of experiments, I investigated various possible neuroendocrine alterations associated with nutritional infertility and I found the following. Increasing circulating levels of estradiol can increase lordosis durations in fasted animals, but the suppression of estrous behavior occurs despite increased circulating estradiol levels in ovariectomized, steroid-treated animals. Next, I found that it takes more than 24 h of metabolic inhibitor administration to inhibit lordosis, whereas only 6 h of refeeding is sufficient to restore sexual receptivity. Furthermore, neither plasma insulin nor leptin levels parallel the changes in estrous behavior, suggesting that changes in circulating leptin and insulin probably do not play a critical role in these behavioral changes. Finally, several conditions that inhibit female sexual behavior are thought to be associated with altered corticotropin-releasing hormone (CRH) activity in the brain. Intracerebroventricular (ICV) infusion of CRH or urocortin inhibited estrous behavior in ovariectomized steroid-primed hamsters. Conversely, ICV infusion of the potent CRH receptor antagonist, astressin, prevented the suppression of estrous behavior by food deprivation. Furthermore, astressin blocked the inhibition of estrous behavior by ICV administration of neuropeptide Y and CRH but did not enhance estrous behavior in animals given an inadequate dose of progesterone. Astressin treatment also induced sexual receptivity in nonresponders, animals that do not normally come into heat when treated with hormones. This effect persisted in subsequent weekly tests in the absence of any further astressin treatment. Manipulations that altered sexual behavior did so without affecting food intake and, in most cases, without affecting circulating corticosteroid levels, indicating that the animals were neither ill nor stressed. These results support the hypothesis that endogenous CRH receptor signaling mediates the inhibition of estrous behavior by undernutrition and in other instances of sexual dysfunction suggesting that CRH receptor signaling may be a final common pathway by which a number of distinct conditions inhibit female sexual behavior.
| Identifer | oai:union.ndltd.org:UMASS/oai:scholarworks.umass.edu:dissertations-3668 |
| Date | 01 January 2002 |
| Creators | Jones, Juli Erin |
| Publisher | ScholarWorks@UMass Amherst |
| Source Sets | University of Massachusetts, Amherst |
| Language | English |
| Detected Language | English |
| Type | text |
| Source | Doctoral Dissertations Available from Proquest |
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