Role of Environmental Factors in Affective, Immune, and Cognitive Processes in Seasonally Breeding Rodents

Non-tropical climates are characterized by annual fluctuations in ambient conditions. During winter food availability and temperatures are reduced compared to summer. Small, seasonally-breeding rodents have evolved traits to maximize reproductive output during the summer, when conditions favor parental and offspring survival, and traits that enhance winter survival of individuals. In this dissertation, I describe a series of experiments focused on investigating the effect of day length (a cue to approximate seasonal changes in rodents), on several seasonally fluctuating traits: immune function, spatial learning, and stress and depressive-like responses. Chapter 1 serves as a review of potential animal models of seasonal affective disorder (SAD), which is a seasonally fluctuating psychological disorder in humans. I describe in Chapter 2 that a lack of melatonin in utero alters behavior in adulthood which suggests that melatonin in early life organizes brain and behavior. Manipulation of melatonin in utero may be useful for investigating season-of-birth variations in human psychological disorders. In Chapters 3 and 4, I describe two studies investigating the interaction of photoperiod and other environmental factors, such as social housing and environmental enrichment, on cell-mediated immune function. Two competing hypotheses describe short-day bolstering of swelling responses to antigenic stimuli: the ‘winter immunoenhancement’ hypothesis and the ‘resource allocation’ hypothesis. These studies are aimed at dissociating whether short-day-induced increases in cell-mediated immune function are due to an endogenous bolstering of immune function, due to energetic trade-offs, or a combination. In chapter 5, I describe how photoperiod influences HPA axis reactivity and circadian pattern in cortisol secretion. As noted, stressor load varies across a year and hamsters may modulate HPA axis functioning to increase their ability to cope with increased stressor load in the winter. Reactivity may also explain photoperiod-related changes in depressive-like responses. Although photoperiod did not induce gross changes in stress reactivity, an acute stressor disrupted the typical afternoon peak in cortisol concentrations. Finally, in chapters 6 and 7, I describe how environmental factors, such as photoperiod and environmental enrichment, can induce structural changes in the brains, specifically, the hippocampi, of seasonally-breeding Siberian hamsters and white-footed mice. These hippocampal changes are functionally relevant as they correspond with spatial learning in white-footed mice and depressive-like responses in Siberian hamsters. These studies may contribute to our understanding of SAD. SAD may originate from the extended duration of nightly melatonin secretion during fall and winter, in common with seasonally-fluctuating traits in temperate-dwelling rodents. Current research in depression and animal models of depression suggests that hippocampal plasticity may underlie the symptoms of depression and depressive-like behaviors, respectively. In sum, investigating photoperiod-induced fluctuations in immune function, cognition, and depressive-like and stress responses may help elucidate seasonal fluctuations in human disease, cognition, and affect.