Cognition, defined as the mechanism by which an animal acquires, processes, stores, and uses information present in the environment, is a trait that is sensitive to developmental conditions. Existing research supports the idea that the ability to develop and maintain cognitive abilities depends on the physiological condition of the individual, which can be influenced by the early environment. Alterations in maternal care, social stress, and malnutrition are some examples of environmental conditions that impact development and resulting cognitive abilities across taxa. The primary goal of this research was to determine whether immune system challenge during the critical song learning period in zebra finches (Taeniopygia guttata) would lead to long term negative impacts on song quality and learning, spatial learning, and neophobia. Immune challenge during this period of development did not produce long term impacts on learning or memory, nor did it lead to any changes in neophobic responses. However, birds that were hatched later in a clutch performed better on the motoric and spatial tasks, and were less neophobic. Future research in zebra finches that can describe the variation in song attributes as a function of hatching order would be a useful first step in determining a mechanistic link between hatch order and song learning outcomes. / Master of Science

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Dissertation (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2008. / Vita. Bibliography: p. 96-110.

During adolescence, animals leave the natal home and interact with potentially threatening stimuli (i.e. stressors), e.g. unfamiliar environments and conspecifics. Adolescent stressors can result in fewer interactions with unfamiliar stimuli in adulthood, plausibly due to sustained effects of glucocorticoid exposure on stress physiology (e.g. glucocorticoid secretion and receptor expression). The current thesis tested the hypothesis that adolescent glucocorticoid exposure and social experiences act as stressors by quantifying the effects of the adolescent experiences on behavioural responses to unfamiliar stimuli and the underlying neuroendocrine mechanisms when in adulthood using two captive species, zebra finches and rats. In study one, adolescent zebra finches were dosed with the glucocorticoid corticosterone. In adulthood, birds dosed with corticosterone in early adolescence took longer to enter an unfamiliar environment when tested individually and had lower expression of the glucocorticoid receptor GR in the hippocampus and hypothalamus, brain regions that regulate stress responses. Glucocorticoids therefore appear to be an endocrine mechanism behind the long-term effects of adolescent stress. Subsequent studies explored whether higher social density and more unfamiliar social interactions during adolescence act as stressors. In study two, early adolescent zebra finches were housed in groups varying in conspecific number and density. In adulthood, females raised in larger groups secreted a higher stressor-induced corticosterone concentration and, if raised at lower density, spent more time in an unfamiliar environment when group housed. In study three, adolescent female rats were housed in familiar pairs or exposed to unfamiliar conspecifics. Unfamiliar adolescent interactions had no effects on responses to unfamiliar environments or stress physiology in adulthood, but heightened ultrasonic call rates. In this thesis, adolescent social experiences do not act like stressors, but modulate (especially female) social behaviour. Adolescent stressors and social experiences therefore have distinct effects on responses to unfamiliar stimuli and stress physiology that are maintained into adulthood.

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Throughout their lives, animals are faced with numerous ecological challenges stemming from abiotic and biotic conditions of their environment. Phenotypic shifts in response to one challenge can have cascading effects on other organismal systems, with downstream implications for individual fitness. Infectious disease presents a significant ecological challenge for most organisms on earth. Additionally, how an animal responds to disease can be shifted by exposure to other ecological challenges. Thus, infectious disease can both present an ecological challenge itself or shift as a consequence of another challenge. In this work, I used experimental captive studies on wild-caught house finches (Haemorhous mexicanus) to elucidate how an animal might shift its phenotypes when presented with an ecological challenge. In the first experiment, I examined how nutritional stress during nestling development impacted the magnitude of house finch responses to the bacterial pathogen Mycoplasma gallisepticum (MG). Although nutritional stress limited mass gain in nestlings, individual responses to MG did not vary with nutritional stress, possibly indicating that the development of immune responses is resilient even in the face of suboptimal nutritional conditions. Next, I investigated infectious disease as a challenge in itself and asked how individual social preferences were shifted by MG infection. I demonstrated that MG-infected house finches showed augmented sociality relative to control birds, choosing to spend more time with a group of conspecifics than alone. Because this increased social preference was no longer present once birds recovered, this phenotypic change in sociality may have specific benefits for actively infected birds. Finally, my last experiment expands upon these results, exploring whether group-living particularly benefits infected birds by offsetting two common fitness costs of infection: reduced foraging abilities and decreased anti-predator responses. Here we found that group-living provides all individuals with improved foraging and anti-predator behaviors, with the strongest benefits of group-living apparent for infected finches. This suggests that augmented sociality in infected house finches has important implications for surviving infection, and potentially, for the spread of MG within populations. As animals continue to face increasing and novel ecological challenges, it is vitally important to understand individual responses to environmental challenges, which can have long-term effects for all levels of biological organization. In particular, my work highlights the role of social behavior as a potentially adaptive phenotypic response to infectious disease in wild animals. Taken together, my results demonstrate the importance of continuing to study infectious disease from multiple perspectives to better understand how animals will respond to a shifting world. / Doctor of Philosophy / All animals must respond to challenges in their environment, which can impact their lives in a variety of ways. Infectious disease is a significant challenge for most organisms on earth. Infection with a disease-causing pathogen must be met by the individual with behavioral, physiological, and immunological responses to increase the animal's likelihood of survival. Additionally, an animal's response to disease can be shifted by exposure to other adverse environmental conditions, such as reduced access to food. On the one hand, infectious disease can present a challenge in itself. Alternatively, how an animal responds to disease may shift as a consequence of another challenge. In this work, I brought wild-caught birds into a captive setting and performed three experiments to determine how an animal might respond to common ecological challenges. First, I studied how food shortages during early life impacted how strongly birds responded to infection with a disease-causing bacteria. In this study I found that host responses to disease did not shift, even when birds were given less food and experienced reduced mass growth during early life. Although young animals are developing rapidly and are particularly vulnerable to challenges in their environment, my results indicate that the development of responses to disease is resilient even in the face of suboptimal conditions. Next, I investigated how social behaviors were shifted due to disease. Here I demonstrated that diseased birds were more social than healthy birds, preferring to spend more time with a group of other birds than alone. In contrast, once these same birds had recovered from infection and were again healthy they became less social, which suggests that diseased birds in particular may benefit from being part of a group. My final experiment expanded upon these results, exploring whether group-living can help increase an individual's survival by compensating for two consequences of disease: reduced ability to acquire food and evade predators. Here I found that group-living provides individual benefits in terms of both acquiring food and evading predators, both of which have important implications for an individual's survival, especially while experiencing disease. As animals continue to face increasing and new challenges due to global change, it becomes vitally important to understand individual responses to environmental changes. While the work highlighted here presents an important step in understanding individual responses, future work should use observational studies in the wild to determine how the social preferences and behaviors I demonstrated here are actually occurring in a natural habitat. Taken together, my results highlight the importance of continuing to study infectious disease from multiple perspectives to better understand how animals will respond to a shifting world.

Crocodilians and birds comprise sister taxa of archosaurs, the development of these vertebrates occurs within an egg case that leaves developing embryos susceptible to fluctuations in the nesting environment. Studies suggest that sub-optimal conditions alter morphological growth and cardiovascular physiology. Regulation of the cardiovascular system is immature in the subjects studied, and embryos may rely on humoral rather than neural control of the cardiovascular system. The primary focus of this dissertation was to assess regulatory mechanisms responsible for maintenance of arterial pressure and heart rate. Dehydration stress had marked effects on embryo growth, and altered baseline cardiovascular parameters, while leaving the response to humoral regulator, angiotensin II (Ang II), unaffected. However, dehydrated alligator embryos developed cholinergic tone on heart rate. Hypoxic incubated chicken embryos were reduced in embryo mass, and altered response to humoral regulatory components Ang I and adenosine in addition identifying a novel regulatory component of the cardiovascular response to acute hypoxia. Collectively, these studies add to the existing knowledge of cardiovascular physiology in embryonic archosaurs and suggest that some components of cardiovascular regulation are plastic following developmental stress.