Female and male rats are often described as having a promiscuous mating strategy, yet simple Pavlovian conditioning paradigms, in which a neutral odor or strain-related cues are paired with preferred sexual reward states during an animal's first sexual experiences, shift this strategy toward copulatory and mate preferences for partners bearing the familiar odor or strain cue. We examined whether female rats given exclusive rewarding copulation with one particular male would display mate-guarding behavior, a strong index of monogamous mating. Ovariectomized, hormone-primed female Long-Evans rats were given their first 10 paced sexual experiences at 4-day intervals with a particular unscented male of the same strain. A final test was conducted in an open field 4-days later in which the primed, partnered female was given access to the male partner and a fully-primed competitor female. In this situation, the partnered females mounted the competitor female repeatedly if she came near the vicinity of the male. This behavior prevented the male from copulating with the competitor, and was not displayed if partnered females could not pace the rate of copulatory behavior efficiently during the training trials, nor was it displayed by the competitor females. Fos expression was examined in both the partnered and competitor females after the final open field test. Partnered females had significantly higher expression within the supraoptic nucleus and nucleus accumbens shell compared to partnered females that did not develop this behavior or competitor females. These data show that females engaged in paced copulation with the same male display mate-guarding when exposed to that male and a competitor female. Increased activation of the SON and NAc may underlie this behavior.
Parkinson's disease (PD) is a multifactorial condition arising from a constellation of environmental insults in conjunction with genetic vulnerabilities, sex differences, and aging. The objective of the current thesis was to explicate potential additive/synergistic effects of genetic LRRK2 anomalies and environmental risk factors as they pertain to motor behaviour, nigrostriatal dopaminergic degeneration, and indices of neuroinflammation. Moreover, since the male sex represents a significant risk factor in PD, sexual dimorphisms were addressed. To achieve this, male and female mice bearing the G2019S-LRRK2 mutation were exposed to a systemic lipopolysaccharide (LPS) + paraquat (PQ) neurotoxicant challenge. Contrary to expectations, no additive/synergistic effects were observed between the G2019S mutation and LPS+PQ exposure. In fact, male G2019S mice appeared to be protected from the degenerative effects of LPS+PQ at this age. Moreover, an unanticipated sex by treatment interaction was found, such that female mice displayed greater deficits in gait and greater loss in nigral TH-positive neurons compared to males. SEX AND LRRK2 GENOTYPE DIFFERENCES IN PDiii Acknowledgements
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