Narcolepsy is a neurological disorder characterized by a person’s inability to regulate sleep-wake cycles. Excessive daytime sleepiness and cataplexy are prominent symptoms of narcolepsy. Cataplexy is partial to full body muscle atonia usually brought on by the person with narcolepsy experiencing a positive emotion. Some features of cataplexy resemble those of REM sleep, including similar brain activity and muscle atonia. The neuronal circuit that produces cataplexy has yet to be determined. The similarities between REM sleep and cataplexy support the hypothesis that cataplexy is the result of the REM atonia pathways being activated. An emotion processing region, the central amygdala (CeA), projects to known REM regulatory regions and plays a role in cataplexy. GABAergic neurons of the CeA are sufficient and necessary to trigger cataplexy in mice and project to brainstem regions that regulate muscle tone. Cataplexy is often triggered in a social setting, such as when seeing an old friend or telling a joke. Oxytocin (OT) is involved in many social behaviors, making it a viable link between social stimuli and cataplexy. We hypothesized that oxytocin receptor (OTR) neurons of the CeA, a sub-population of GABAergic neurons, promote emotionally-triggered cataplexy. To determine the social phenotype of the narcolepsy mouse model, the orexin knock-out (OXKO) mouse, we used established behavioral assays of social interaction and social memory. To determine if social reunification influenced the amount of cataplexy, group-housed OXKO mice were isolated for a short time and reunited with their littermates. To determine if OTR neurons of the CeA were sufficient and necessary to promote socially-triggered cataplexy, we used chemogenetic technology known as Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to selectively activate or inhibit these neurons. We injected adeno-associated viral vectors coding for either the excitatory hM3 Cre-dependent DREADD or the inhibitory hM4 Cre-dependent DREADD into the CeA of orexin knock-out mice crossed with OTR-Cre mice, allowing for expression of the DREADD exclusively in the OTR neurons of the CeA. After injection with either saline or clozapine-N-oxide (CNO) we put the mice through a behavioral assay to see if emotionally-triggered cataplexy increased or decreased following the activation or inhibition of OTR neurons of the CeA. The behavioral assays showed that acute social interactions in OXKO is normal, however they do have a social memory impairment. In addition, reunification promotes cataplexy in most OXKO mice. With the chemogenetic experiments, our number of mice is too low to report if OTR neurons of the CeA are sufficient and/or necessary for cataplexy at this time. / 2020-07-03T00:00:00Z

The ways that individuals socialize within groups have evolved to overcome challenges relevant to species-specific socioecology and individuals’ life history state. Studying the drivers, proximate benefits, and fitness consequences of social interaction across life stages therefore helps clarify why and how social behavior has evolved. To date, juvenility is one life stage that field researchers have largely overlooked; however, individual experiences during development are relevant to later behavior and ultimately to fitness. Juvenile animals are subject to unique challenges related to their small size and relative inexperience. They are likely to employ behavioral strategies to overcome these challenges, while developing adult-like behavioral competence according to their species and sex. The research presented in this dissertation draws from long-term behavioral records of adult females and shorter-term behavioral records of juveniles from a population of blue monkeys (Cercopithecus mitis stuhlmanni) in western Kenya. I combine data on social behavior, demography, and biomarkers related to energetic and metabolic status, to assess both short and long term corollaries of social strategies in this gregarious Old World primate. I first explored whether the quality of social ties predicted longevity among adult female blue monkeys. Controlling for any effects of dominance rank, group size, and life history strategy on survival, I used Cox proportional hazards regression to model the both the cumulative and current relationship of social ties and the hazard of mortality in 83 wild adult females of known age, observed 2-8 years each (437 subject-years) in 8 social groups. The strength of bonds with close partners increased mortality risk under certain conditions: females that had strong bonds with partners that were inconsistent over multiple years had a higher risk of mortality than females adopting any other social strategy. Within a single year, females had a higher risk of mortality if they were strongly bonded with partners that were inconsistent from the previous year vs. with partners that were consistent. Dominance rank, number of adult female group-mates, and age at first reproduction did not predict the risk of death. This study demonstrates that costs and benefits of strong social bonds during adulthood can be context-dependent, relating to the consistency of social partners over time. To understand the adaptive value of social behavior among juveniles, it was first necessary to understand the conditions under which their social behavior occurred and with which it co-varied. I examined the social behavior of 41 juvenile blue monkeys, using data collected over 8 consecutive months. I analyzed variation in social activity budgets and partner number related to life history characteristics, socio-demographic conditions, and seasonal environmental change. I examined partner preferences according to kinship, and relative age and rank. Lastly, I explored the stability of juvenile social tendencies over time. Males and females differed strongly in their social activity budgets and partner numbers: males spent more time playing with more partners than females, whereas females spent more time grooming and sitting close with more partners than males. Nevertheless, they were much more similar in terms of their partner preferences. Juveniles generally preferred to interact with partners with whom they were closely related and that were similar in age and maternal rank. Juveniles’ affiliative and aggressive behavior varied seasonally, suggesting that these two types of behavior were related. Rates of agonism given and received were the only types of social behavior to demonstrate repeatable inter-individual differences. This analysis provides a comprehensive examination of juvenile behavior in blue monkeys, synthesizing findings with those in other primate and non-primate species. I then explored the short-term costs and benefits of juveniles’ sociality in terms of their effects on allostatic load. I examined variation in energy balance (as measured by urinary C-peptide), social style, and their influences on allostatic load (as measured by fecal glucocorticoid metabolites, fGCs). Juvenile energy balance varied according to sex, availability of ripe fruit, and rainfall. Both energy balance and social style predicted fGC levels, such that juveniles that had a higher energy balance, groomed less, and played more had lower fGCs. Time spent grooming interacted with energy balance in their effect on fGCs, such that individuals with higher energy balance actually had higher fGCs the more time they groomed. Neither maternal rank nor involvement in agonism corresponded with juvenile fGC levels. These results suggest that juvenile blue monkeys experience energetic stressors and that navigating the social environment via overt affiliative behavior, namely grooming, is a potentially stress-inducing endeavor. Lastly, to further understand variation in social behavior during juvenility, I explored the role of mothers in shaping juveniles’ affiliative tendencies. I examined whether the social behavior of juvenile animals resembled that of their mothers and whether their social behavior was subject to maternal effects, using data from the 41 juveniles and their 29 mothers. Juveniles’ grooming time with peers corresponded with the amount of time they groomed with (primarily being groomed by) mothers as infants, and this relationship varied by sex. Females spent less time grooming with peers the more maternal grooming they received during infancy, whereas males groomed with peers more. The time juveniles spent in other types of association with partners did not correspond with the same behavior in mothers, nor were other types of association subject to maternal effects. This exploratory study suggests limited effects of maternal behavior during infancy, but also that females and males respond differently to maternal investment during the first year. The results of this dissertation emphasize the importance of long-term studies of natural populations in understanding the evolution of social behavior, particularly when examining the causes and consequences of social ties over the life cycle in a long-lived animal. Strategies of affiliation did indeed correspond with costs and benefits over the life cycle, as they were relevant both to mortality in female adults and metabolic hormones among juveniles. Further, individuals socialize during development according to their life trajectory as male or female, what seasonal changes in the physical environment require or allow, and early-life maternal effects.

The current studies examined the interplay of dominance and power in their effects on various forms of prosociality, along with potential mechanisms that may account for their differential effects. Study 1 found that dominance and power had opposing effects on general prosocial tendencies, with dominance negatively relating to and power positively relating to general prosociality. Study 2 found the negative effects of dominance to be consistent both for general and relationship-specific prosociality. The effects of power were not replicated for the outcomes shared with Study 1, but other positive associations were found between power and prosocial propensities. Indirect effects in studies 1 and 2 supported the potential mediating role of other focus in explaining the differential effects of dominance and power. Study 3 utilized an experimental design to directly examine the potential mediating role of other-focus, by manipulating independent versus interdependent self-construals. Significant interactions between power and condition supported the notion that power positively affects prosociality by increasing other-focus. In the interdependent condition, power significantly predicted perspective-taking, whereas in the independent condition, the effect of power on perspective-taking was not significant. Study 4 involved collecting dyadic data from romantic partners, but did not find any significant partner effects. In line with the other studies, dominance was negatively associated with self-reported supportive tendencies as well as self-reported perceptions of a partner’s supportive behaviors. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2019. / FAU Electronic Theses and Dissertations Collection

A group of four captive bobcats (Felis rufus), two males and two females, was observed for 102.67 hours over the period of one year. A pilot study was conducted consisting of a minimum of three separate observations for each daylight hour. The remaining observations were concentrated during the early morning hours immediately after feeding, the time of maximum activity and social interaction.

Thesis (Ph. D.)--University of Washington, 1985. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--School of Psychology, Georgia Institute of Technology, 2004. Directed by Terry L. Maple. / Vita. Includes bibliographical references (leaves 213-226).

Section A explores the insights offered by the qualitative literature to our understanding of staff responses to challenging behaviour within services for people with intellectual disabilities. The trustworthiness of the literature is examined. The studies are reviewed using the cognitive-emotional model as a guide and allowing for other themes to emerge. The review concludes with a discussion of the implications for future research and clinical practice. Section B reports on a pilot study investigating staff reactions to challenging behaviour within services for people with intellectual disabilities. This study sought to explore the development of staff cognitive, emotional and behavioural responses to challenging behaviour over the course of challenging interactions. Video elicitation interviews were conducted with six staff members responding to the challenging behaviour of two service users. Interview data were subject to content analysis and an attributional analysis in order to assess their cognitive and emotional responses as they were at the time. In addition, staff behaviour was subject to descriptive and sequential analyses to explore their relationship with cognitive-emotional variables. Results indicated that staff experienced a wide range of cognitions and emotions during challenging interactions. Cognitions varied over the course of an incident. A tentative relationship was found between internal attributions of challenging behaviour, negative emotions and verbal responses by staff. Staff members spontaneously made causal attributions of service user behaviour during challenging interactions. Rather than being a stable attribute of the staff member, attributions seem to vary to a degree across the course of an interaction. This has implications for both research and clinical practice.

Reciprocal changes in UBE3A gene dosage cause two neurodevelopmental disorders. Maternally inherited deletions of UBE3A cause Angelman syndrome, characterized by intellectual disability, motor defects, seizures, and a pathognomonic increased social motivation. Whereas maternally inherited triplications of UBE3A as in Idic15 Autism underlie decreased sociability and increased repetitive restrictive behaviors of this disorder. Identifying the cellular compartments and neuronal subtypes where excess and loss of Ube3a impair behavior is essential to understanding and potentially treating the disorders. In Chapter 2, we show that mouse models of maternal loss of UBE3A (Ube3a-mKO, Angelman syndrome) and triplication of UBE3A (Ube3a-2x, Idic15) have opposite effects on social behavioral and cortical gene expression. Social preference and social vocalizations are reduced in Ube3a-2x and increased in Ube3a-mKO mimicking the human phenotypes. Using a nuclear localizing signal tagged Ube3a transgenic mouse (Ube3a-NLS), we show that Ube3a acts in the nucleus to impair social behavior and cortical gene expression. Many of the genes reciprocally regulated by nuclear Ube3a are part of an Autism protein-interaction network. In Chapter 3, we demonstrate Ube3a-2x mice have increased aggression, an important Autism comorbidity. In contrast, maternal loss of Ube3a reduces aggression, consistent with the gregarious, amiable nature of individuals with Angelman syndrome. We then mapped the loci where increased Ube3a increases aggression. Increased aggression was observed when Ube3a was targeted to glutamatergic and vasopressinergic but not to GABAergic or oxytocinergic neurons. In Chapter 4, we show that in mice, social behavior is downregulated by social experience via Ube3a. In wild-type mice, altering their social environment strongly regulates their social behavior: individual housing causes hypersocial whereas group housing causes hyposocial behavior. In Ube3a-2x animals, group housing caused an excessive downregulation of social behavior whereas single housing fully rescued their social behavior deficits. By contrast, in Ube3a-mKO animals, the suppressive effects of group housing on social experience was largely blocked, suggesting Ube3a is required for this process. In summary, this thesis characterizes the role of UBE3A gene dosage in regulating social and aggression behaviors and identifies the subcellular compartment and neuronal subtypes where changes in Ube3a gene dosage disturb the homeostasis of these behaviors.

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