Thesis (Ph.D.), Memorial University of Newfoundland, 2000. / Includes bibliographical references.

No description available.

More than half of known crime is committed by 5-6% of the criminal population. Who are these people? Research has shown that it is likely that a majority of these individuals are characterized by having a psychopathic personality. Interestingly, research has shown that psychopathic features are not unique to adults. Youths with high levels of psychopathic traits resemble adult psychopaths in that they are the most frequent, severe and aggressive, delinquent offenders. There is less knowledge, however, about the development of these traits in adolescence, and many fundamental questions have yet to be addressed. The aim of this dissertation is to begin to examine a few of these questions, such as: a) the role of parents andtheir behavior in the development of psychopathic personality in adolescence; b) patterns of stability and change in psychopathic traits during adolescence; and c) whether or not subgroups of adolescents with high levels of psychopathic traits can be identified in a normative community sample. Overall, the results reveal that a psychopathic personality profile characterizes a small group of youths at particular risk of negative development. This group, as well as showing high levels of psychopathic traits throughout adolescence, report high levels of delinquent behavior, and also experience dysfunctional relationships with their parents. Further, the results reveal important subgroups of adolescents with high levels of psychopathic traits, much in accordance with the literature on adult psychopaths. Whereas one group expresses the personality style of primary psychopaths, another is more aggressive, impulsive, and anxious than the other. Taken together, the results of this dissertation suggest that some adolescents are at particular risk of future negative development. Implications for theory and practice, and for the directions of future research, are discussed.

Maternal behavior in rodents is dependent, at least in part, on prolactin acting in the brain. Pheromones carried by male mouse major urinary proteins lower serum prolactin levels in female mice. Therefore, we hypothesized that virgin female C57BL/6J mice housed in split cages, where they had pheromonal but not physical contact with a male, would show suppressed maternal behavior. Contrary to our hypothesis, we found split-cage housed females were significantly faster to retrieve 3 foster pups on the first and second day of maternal behavior testing compared to mice housed in individual cages. The advancement in maternal behavior was replicated when virgin females were simply exposed to male mouse urine-soaked bedding. Ovariectomising the mice, to remove the influence of steroid hormones, prior to placement in the split cages, prevented the pheromonal advancement of maternal behavior. The data infer that an ovarian steroid-dependent action of male mouse pheromones primes virgin female mice to express maternal behavior more rapidly when mouse pups are introduced. This effect required greater than 14 days exposure to male pheromones. Male mouse pheromones are reported to suppress prolactin secretion. However, serum prolactin levels in split-caged housed females, where they had pheromonal but not physical contact with a male, were only briefly lowered and became significantly elevated from 24 hours until 72 hours of pheromonal contact. Despite the early increases in prolactin after pheromone exposure, levels were significantly lower in the pheromone-exposed females when maternal behavior was tested after 21 days. It has been previously reported that prolactin is important in the onset of maternal behavior, but is not required for the ongoing maintenance of maternal behavior. We hypothesised that the hyperprolactinemia observed in the first 24-72 hours of pheromonai exposure had subsequently led to the enhanced maternal behavior. To test this we injected a group of individually-housed mice with slow release prolactin for 48 hours to simulate the period of hyperprolactinemia, and blocked prolactin secretion in a group of split-caged housed females with bromocriptine, and tested their maternal behavior 18 days later. The mice injected with prolactin had enhanced maternal behavior, compared to controls injected with a placebo. By contrast, bromocriptine inhibition of prolactin secretion completely prevented the pheromonal enhancement of maternal behavior. This suggests that the pheromonal advancement of maternal behavior is specifically mediated by a 48-hour period of sustained hyperprolactinemia. It has been previously shown that pregnancy increases neurogenesis in the subventricular zone in a prolactin-dependent manner. Therefore, as the male pheromone-induced advancement of maternal behavior is prolactin-dependent and takes some time to occur, we hypothesized that long-term pheromonal contact initiates mitogenesis in the subventricular zone. Split-caged housed mice showed a significant increase in BrdU-labeled cells in the subventricular zone after 7 days of contact which reduced to baseline levels by 14 days of contact. The mice injected with BrdU on day 7 of contact and killed 21 days later showed a significant increase in labeled cells in the accessory olfactory bulb compared to controls. The data suggest that male mouse pheromones initiate mitogenesis in the subventricular zone of virgin C57B6 mice, in an exposure-dependent manner, and that these cells travel via the rostral migratory stream to the accessory olfactory bulb. As with the effect on maternal behavior, the pheromone-induced increase in neurogenesis was steroid- and prolactin-dependent. During pregnancy and lactation in rodents, prolactin receptor expression is increased in the MPOA, an adaptive change, which could lead to an increased neuronal response to serum prolactin levels, which are high just prior to parturition, and consequently could underlie the enhanced maternal responses seen in late pregnancy and after parturition. It is known that systemic prolactin can access the brain, but it is also possible that there could be local synthesis of brain prolactin acting in an autocrine or paracrine manner. Therefore we hypothesized that the pheromonal-induced changes in maternal behavior are being mediated by altered prolactin receptor expression/sensitivity and/or increased production of brain prolactin. Using RT-PCR to measure levels of prolactin receptor and prolactin mRNA, we found changed expression of the 3 short forms and the long form of prolactin receptor mRNA in the arcuate nucleus, paraventricular nucleus, bed nucleus of the stria terminalis, and MPOA with either exposure to male pheromones or pups. We also found changes in prolactin mRNA in the MPOA and paraventricular nucleus after exposure to pups or male pheromones. The data suggest that altered levels of expression of the receptor, coupled with local production of brain prolactin acting in an autocrine or paracrine manner, may cause a net change in prolactin cell signaling, which leads to adaptive responses which ensure reproductive success. There is extensive evidence that dopamine is a key neurotransmitter mediating maternal behavior. In addition, there is some evidence that serotonin may also be involved in regulating maternal behavior. Therefore, we hypothesised that the pheromonal-induced changes in maternal behavior would be associated with increased dopaminergic and/or serotonergic neuronal activity in the MPOA and other areas of the brain implicated in maternal behavior expression. Using HPLC to measure levels of dopamine and serotonin and their respective metabolites, we found a significant increase in serotonergic and dopaminergic neuronal activity in the MPOA of virgin female C57BL/6J mice after 24 hours of pheromonal contact. The neuronal activity returned to basal levels after exposure to pups. The data suggest that male mouse pheromones increase serotonergic and dopaminergic neuronal activity in the MPOA, but that dopamine and serotonin levels are tightly regulated within strict parameters dependent on what physical stimuli the female is receiving. Changes in prolactin levels are associated with altered responses to anxiety. There is an increased risk of anxiety and depression with sustained periods of hyperprolactinemia, and in the postpartum period, where there are fluctuations in prolactin levels, there is an increased risk of mood disorders. As pheromones change both serum and brain prolactin levels and prolactin modulates anxiety, we hypothesised that female mice exposed to pheromones would show altered behavioral responses to a standardized test of anxiety. We found that male pheromone-exposed mice showed decreased levels of anxiety on an elevated plus maze compared to individually housed controls. Female mice exposed to female pheromones displayed 2 disparate responses to the plus maze. One female from each cage showed increased anxiety, while her cage-mate showed decreased anxiety, yet both groups of female mice showed impaired maternal behavior. We infer, that in this model, male pheromones decrease anxiety, but anxiety and expression of maternal behavior are not directly correlated. The major signal transduction pathway activated by prolactin binding to its receptors in the brain is the JAK/STAT signalling pathway, and in some neurons, in particular, the STAT5B pathway. The expression of prolactin and its receptor affect maternal behavior in mice. Therefore, we hypothesised that if the JAK/STAT STAT5B pathway is involved in maternal behavior, then STAT5B-deficient mice would have altered maternal behavior. We found that there were no significant differences in expression of full maternal behavior between the STAT5B-deficient mice and wild-type controls. The data suggest that STAT5B is not required for normal expression of maternal behavior. We propose that the prolactin-mediated pheromonal increase in neurogenesis, alteration in monoamine synthesis, and alteration of prolactin and prolactin receptor mRNA levels facilitate expression of enhanced maternal behavior. We further propose that the pheromonal decrease in anxiety does not mediate enhanced maternal behavior. In addition, we propose that prolactin does not mediate maternal behavior through STAT5B. While pheromones have previously been reported to exert powerful actions on the reproductive system, these results demonstrate for the first time that male pheromones potentially complement the prolactin-mediated establishment of maternal behavior.

In this thesis my initial goal was to use yellow warblers to examine the effect of paternal care on female mate choice. I first examined whether mate choice based on paternal care could be considered adaptive. Paternal care was variable among males and important to female fitness, but, contrary to a previous report, male chest striping could not be used to predict paternal care. Females did not compensate for reductions of male parental care, which resulted in significantly reduced nestling growth. In chapter two I tested the idea that monogamy in birds is maintained because of the need for biparental care. I reduced the need of strict biparental care by providing pairs at some nests with supplemental food, and found that the main effect of supplemental food was on maternal, not paternal behaviour. The first two chapters suggest that males and females provide for their brood independently from each other, which is in disagreement with current models on the maintenance of biparental care. These models assume that any given factor must affect maternal and paternal care equally for biparental care to be maintained. In Chapter three I showed that the effects of brood size and nestling age on parental care are similar for both sexes. In Chapter four I deal with age-related changes in reproductive success and the possible effects on female mate choice. Age affected the likelihood of breeding in females, but only the time of breeding in males. These changes were accompanied by age-related increases in size in both sexes. These results raise the possibility of age-related increases in parental ability, and female preference for older males.

Thesis (M.A.)--University of Wisconsin--Madison, 1969. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (p. 138-144).

Thesis (PH.D.)--Michigan State University. Zoology Ecology, Evolutionay Biology, and Behavior, 2008. / Title from PDF t.p. (viewed on Aug. 11, 2009) Includes bibliographical references (p. 64-72). Also issued in print.

Thesis (Ph.D.)--Memorial University of Newfoundland, 2004. / Includes bibliographical references.

Thesis (Ph.D.) - University of St Andrews, March 2010.

No description available.