The role of corticotropin-releasing factor in binge-like ethanol consumption

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  • March 21, 2019
Creator
  • Lowery-Gionta, Emily Geyer
    • Affiliation: College of Arts and Sciences, Department of Psychology and Neuroscience
Abstract
  • Previous research establishes a crucial role for corticotropin releasing factor (CRF) in ethanol dependence. Recent evidence demonstrates a role for the CRF type 1 receptor (CRF1R) in the modulation of binge-like ethanol consumption by non-dependent animals, a behavior which can precede ethanol dependence. The goal of this dissertation was to further characterize the role of the CRF system in binge-like ethanol consumption. The role of the CRF receptors in binge-like ethanol consumption were pharmacologically investigated in Chapter 2. In Chapter 3, the effects of binge-like ethanol consumption on CRF expression was assessed using immunohistochemistry techniques. CRF is known to signal through two pathways, the hypothalamic pathway that activates the hypothalamic-pituitary-adrenal (HPA) axis response to stressors, and the extrahypothalamic pathway that includes limbic regions such as the amygdala, which is involved in drug-taking behaviors. Thus, in Chapter 4, the involvement of the HPA axis in binge-like ethanol consumption was assessed using a series of pharmacological and surgical techniques to manipulate HPA axis function and radioimmunoassay techniques to observe the effects of binge-like ethanol consumption on the HPA axis. Based on the results of previous chapters, in Chapter 5, the involvement of the central nucleus of the amygdala was assessed using immunohistochemistry, electrophysiology and pharmacology approaches to manipulate the CRF system. Results show that binge-like ethanol consumption by non-dependent animals selectively alters CRF signaling in the CeA, and that the CRF1R in this brain region is necessary for binge-like levels of ethanol intake to occur. In tandem with data suggesting that the CRF system does not modulate non-binge-like ethanol consumption, these observations suggest that binge-like ethanol consumption, like dependence-induced ethanol consumption, recruits the CRF system of the CeA. Therefore, we hypothesize that recruitment of the CRF system during binge-like ethanol consumption leads to transient neuroadaptations in the amygdala, and these changes in CRF signaling become permanent with repeated binges and eventually culminate in ethanol dependence. The implications of this hypothesis are discussed in the context of the leading theory of alcohol dependence.
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  • "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Psychology (Behavioral Neuroscience)."
Advisor
  • Thiele, Todd
Degree granting institution
  • University of North Carolina at Chapel Hill
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  • Chapel Hill, NC
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  • Open access
Date uploaded
  • March 18, 2013

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