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Psychosocial influences on physiological processes: A focus on health

Norman, Greg

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2010, Doctor of Philosophy, Ohio State University, Psychology.
Social species create emergent organizations beyond the individual that range from pair bonds to colonies to civilizations. These emergent structures likely evolved hand-in-hand with supporting physiological mechanisms as the consequent social behaviors helped these organisms survive, reproduce, and care for offspring sufficiently long to ensure the successful passage of genes to the next generation. Indeed, for many species, inclusion within a social group is essential for survival and its absence represents a significant threat to existence and, as such, engenders pronounced neurobiological, physiological and psychological responses that can have rather dramatic effects on health. The appreciation of this fact has led to the growth of research into the reciprocal interaction between social, psychological and physiological processes. As such, this research represents an interdisciplinary approach devoted to understanding how biological systems modulate, and are modulated by, social processes. In the present dissertation I review my work evaluating the association between psychosocial processes and health in humans and animal models of human disease. I begin by discussing the potent effects of psychological stress on the behavioral and physiological manifestations of peripheral nerve injury, an animal model of chronic neuropathic pain in Chapter 3. In the second section of Chapter 3, I replace chronic restraint stress with chronic social isolation in an attempt to better understand the influence of social factors on neuropathic injury outcome. This study reports that social isolation exacerbates the effects of peripheral nerve injury on depressive-like behavior. Interestingly, this study also found that administration of oxytocin, a hypothalamic neuropeptide associated with social behavior, is capable of mitigating the effects of social isolation on depressive-like behavior in neuropathic animals. Conversely, this study determined that pharmacological interference of oxytocin receptor signaling is capable of blocking the salubrious effects of pair housing on depressive-like behavior following peripheral nerve injury. The first section of Chapter 4 describes my work evaluating the deleterious effects of global cerebral ischemia on acetylcholine neurotransmission and the therapeutic potential of treating ischemic injury with pharmacological agents that target particular acetylcholine receptors known to regulate pathological levels of inflammation. Acetylcholine is a neurotransmitter with broad effects on psychological (e.g. attention, anxiety) and physiological (e.g. autonomic nervous system activity, immune function) processes associated with health. In this study I determined that various cellular components of functional central acetylcholine neurotransmission are dysregulated following cerebral ischemia. In a further demonstration of the important role that cholinergic receptors play in neuroinflammatory and cell death responses, this study also discovered that administration of a selective α7 nicotinic acetylcholine receptor agonist significantly reduced cardiac arrest induced increases in pro-inflammatory cytokine levels as well as microglia and cell death responses within the hippocampus. In the second section of Chapter 4, I discuss my work demonstrating the powerful influence that social isolation can have on behavioral, autonomic, immunological and cell death responses following global cerebral ischemia. Similar to the SNI study described in Chapter 3, socially isolated animals displayed significantly higher levels of inflammation and cell death responses to cardiac arrest in conjunction with displaying more severe dysregulation of the autonomic nervous system and increased depressive-like behavior as compared to pair housed animals exposed to the very same procedure. The next group of studies highlights my attempts to translate portions of the animal work described above into the study of psychobiological processes in humans. In Chapter 5, it was determined that particular patterns of autonomic nervous system functioning are associated with distinct disease states. Consistent with the findings of Chapter 4, patients who displayed relatively low overall autonomic cardiac control were found to be more likely to have previously suffered a myocardial infarction; a finding that, when coupled with the excising literature, suggests that the evaluation of autonomic cardiac control may provide vital information on cardiovascular health status. In Chapter 6, I found that intranasal administration of oxytocin to healthy college age participants selectively increases sympathetic and parasympathetic autonomic cardiac control without altering circulating cytokine or stress hormone levels. Interestingly, this study determined that the effects of oxytocin on autonomic functioning were dependent upon variations within levels of perceived social isolation (loneliness) as lonely individuals displayed limited autonomic responses to oxytocin as compared to nonlonely individuals. Furthermore, as described in Chapter 7, individuals treated with oxytocin displayed significantly lower levels of emotional arousal in response to threatening social stimuli without altering arousal ratings to non-social threat. These latter two studies, coupled with the findings of Chapter 3, provide further evidence that oxytocin has a rather selective influence on social information processing and associated physiological and affective responses. Taken together, the studies described in this dissertation provide a unique perspective on the potential mechanisms that allow psychosocial factors to influence biobehavioral processes and vice verse. Furthermore, these studies highlight some of the strengths of utilizing both clinical and animal research when attempting to understand the mechanisms through which social information is capable of getting under the skin and influencing health.
Courtney DeVries, PhD (Advisor)
Charles Emery, PhD (Committee Member)
Randy Nelson, PhD (Committee Member)
Bennett Givens, PhD (Committee Member)
316 p.

Recommended Citations

Citations

  • Norman, G. (2010). Psychosocial influences on physiological processes: A focus on health [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1280682539

    APA Style (7th edition)

  • Norman, Greg. Psychosocial influences on physiological processes: A focus on health. 2010. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1280682539.

    MLA Style (8th edition)

  • Norman, Greg. "Psychosocial influences on physiological processes: A focus on health." Doctoral dissertation, Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1280682539

    Chicago Manual of Style (17th edition)