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Neural mechanisms mediating persistent stress relief by comfort food

Christiansen, Anne M.
http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275921773

Abstract Details

2010, PhD, University of Cincinnati, Medicine : Neuroscience/Medical Science Scholars Interdisiplinary.
Stress, a real or perceived threat to homeostasis, elicits responses from the HPA axis, triggers the sympathetic branch of the autonomic system, and elicits anxiety-related behaviors. These responses are heavily modulated by forebrain inputs, including the basolateral amygdala (BLA). Palatable food consumption, specifically sucrose snacking, results in collective stress relief, dampening the HPA axis, autonomic, and mood/behavioral responses to stress. In fact, consumption of palatable food is widely used as a kind of “self medication” for stress relief, which may lead to over-consumption and subsequently may contribute to the obesity epidemic. Understanding the mechanisms by which palatable food affects brain regions like the BLA to buffer the stress response may help develop stress interventions without the side-effect of obesity and other weight-related health problems. Using a rat model of palatable snacking, these studies tested the hypothesis that a history of palatable snacking causes persistent alterations in BLA signaling and snacking-induced reductions in the HPA response to stress. These data show that 1) palatable snacking induces numerous indices of synaptic remodeling (i.e. synaptophysin, deltaFosB) in stress and reward brain circuitry; 2) palatable snacking causes a lasting decrease in the hormonal response to stress that is accompanied by persistent alterations in BLA signaling; and 3) calcium calmodulin kinase II alpha (CaMKII) activity within the BLA is not necessary for palatable snacking-induced stress buffering but, in contrast, is responsible for limiting the stress-reducing properties of palatable snacking. The current studies contribute two major ideas to the fields of stress and obesity research. 1) Chronic intake of comfort food causes lasting changes in the brain. In particular, a discrete pathway of forebrain reward and stress regulatory brain regions undergoes synaptic changes after palatable snacking. This work implicates a potential mechanism by which palatable food acts to buffer the stress response. 2) Lasting snacking-induced changes in the brain are paralleled by long-term reductions in the stress response. Once the palatable food-induced stress buffering effects are established, they persist for long periods of time, even after the palatable food intake has ceased. The current studies have important implications for public health by providing insight to neural links between palatable food intake and the stress response. Understanding these endogenous mechanisms could help improve strategies for the prevention and/or treatments of stress-related disorders and obesity.
James Herman, PhD (Committee Chair)
Stephen Benoit, PhD (Committee Member)
David D'Alessio, MD (Committee Member)
Stephen Woods, PhD (Committee Member)
Yvonne Ulrich-Lai, PhD (Committee Member)
176 p.
Neurology
palatable food; stress; brain; plasticity; basolateral amygdala; hypothalamus

Recommended Citations

Citations

  • Christiansen, A. M. (2010). Neural mechanisms mediating persistent stress relief by comfort food [Doctoral dissertation, University of Cincinnati]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275921773

    APA Style (7th edition)

  • Christiansen, Anne. Neural mechanisms mediating persistent stress relief by comfort food. 2010. University of Cincinnati, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275921773.

    MLA Style (8th edition)

  • Christiansen, Anne. "Neural mechanisms mediating persistent stress relief by comfort food." Doctoral dissertation, University of Cincinnati, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275921773

    Chicago Manual of Style (17th edition)

ucin1275921773
531
© 2010, all rights reserved.
This open access ETD is published by University of Cincinnati and OhioLINK.