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Neural and immune changes that occur following psychological and physical stressors

Neigh, Gretchen N.
http://rave.ohiolink.edu/etdc/view?acc_num=osu1092752738

Abstract Details

2004, Doctor of Philosophy, Ohio State University, Neuroscience.
Exposure to stressors can influence the onset and progression of both physical and mental disease, and the effects of stressors on physiology and behavior are, at least in part, mediated by the hypothalamic pituitary adrenal (HPA) axis. The hippocampus is a component of the HPA axis that is susceptible to stressor-induced damage and alterations in the cytoarchitecture of the hippocampus can alter HPA axis function and subsequently immune function. The first series of experiments examined the role of stressor-induced energetic shortage, as signaled by increased concentrations of glucocorticoids, in suppression of immune function and neurogenesis. Mice supplemented with pyruvate, a potent producer of cellular energy, had a lower cumulative exposure to elevated concentrations of glucocorticoids and did not exhibit the restraint-induced suppression of immune function that was evident in restrained mice that did not receive pyruvate supplementation. Pyruvate was not protective against stressor-induced changes in neurogenesis. However, exposure to stressors increased the proportion of proliferating astrocytes in the hippocampus, as compared to neurons. The second set of experiments examined the effects of damage to the hippocampus, by cardiac arrest and resuscitation, on behavior as well as immune function. Cardiac arrest and resuscitation increased anxiety-like behavior, decreased social interaction, and impaired spatial memory. In addition, prior exposure to a restraint stressor augmented post-arrest anxiety-like behavior. The behavioral deficits observed were attributed to hippocampal damage, a reduction in dendritic spines, and an increase in the reactive microglia in the hippocampus. Furthermore, hippocampal damage following cardiac arrest and resuscitation altered HPA axis activity and augmented cell-mediated immune function as compared to mice that were exposed to cardiac arrest and resuscitation but did not sustain brain damage. In addition, the relationship between hippocampal damage and immune function appeared to be bidirectional, as survival following cardiac arrest and resuscitation was compromised in mice that were immunized with a novel protein prior to the cardiac arrest procedure. In conclusion, the work described in this dissertation adds to the body of literature that describes the relationship between the HPA axis and the immune system.
Randy Nelson (Advisor)
A. DeVries (Advisor)
Firdaus Dhabhar (Other)
258 p.
stress; hippocampus; HPA axis; cardiac arrest; psychoneuroimmunology; corticosterone; housing; pyruvate

Recommended Citations

Citations

  • Neigh, G. N. (2004). Neural and immune changes that occur following psychological and physical stressors [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1092752738

    APA Style (7th edition)

  • Neigh, Gretchen. Neural and immune changes that occur following psychological and physical stressors. 2004. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1092752738.

    MLA Style (8th edition)

  • Neigh, Gretchen. "Neural and immune changes that occur following psychological and physical stressors." Doctoral dissertation, Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1092752738

    Chicago Manual of Style (17th edition)

osu1092752738
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© 2004, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.