The role of neuropeptide Y signaling on binge-like ethanol consumption Public Deposited

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  • March 21, 2019
  • Sparrow, Angela Maria
    • Affiliation: College of Arts and Sciences, Department of Psychology and Neuroscience
  • Neuropeptide Y (NPY) is a neuromodulator that modulates a number of neurobiological responses including anxiety and ethanol consumption. The goal of the present studies was to examine the role of NPY in binge-like drinking using the drinking in dark (DID) procedures, which is an animal model of binge-like ethanol consumption using C57BL/6J mice. Experiment 1 involved central administration of NPY and receptor selective agonists and antagonists prior to ethanol exposure to test the hypothesis that NPY Y1 and Y2 receptor signaling have important modulatory roles in binge-like ethanol consumption. The results of this set of experiments indicate that NPY reduces binge-like ethanol consumption through activation of the Y1 receptors or antagonism of the Y2 receptors. Experiment 2 tested the hypothesis that repeated binge-like ethanol consumption alters levels of NPY and NPY receptors by subjecting mice to a varying number of binge-like ethanol drinking cycles followed by immunohistochemistry techniques to assess NPY and Y1 receptor immunoreactivity (IR) in regions of the extended amygdala. NPY and Y1 receptor IR was reduced in the central nucleus of the amygdala (CeA), the bed nucleus of the stria terminalis and the nucleus accumbens in mice exposed to binge-like ethanol consumption compared to water control mice. Based on these results, experiment 3 utilized a neurotoxin conjugated to NPY, which blunts NPY signaling by causing cell death in cells expressing NPY receptors. This neurotoxin was used to test the hypothesis that NPY receptor signaling in the amygdala has a modulatory role for binge-like ethanol consumption. The data revealed that blunted NPY signaling in either the CeA or the basolateral amygdala blocked the reduction of binge-like ethanol consumption by centrally administered NPY. Taken together, these experiments indicate that NPY has modulatory role for binge-like ethanol consumption through Y1 and Y2 receptors in the extended amygdala. Furthermore, binge-like ethanol consumption produces transient alterations in the NPY system, which may lead to the development of ethanol dependence. These results also suggest a possible therapeutic value for NPY to protect against excessive ethanol consumption and the development of ethanol dependence.
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  • In Copyright
  • "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Psychology (Behavioral Neuroscience)."
  • Thiele, Todd
Degree granting institution
  • University of North Carolina at Chapel Hill
Place of publication
  • Chapel Hill, NC
  • Open access

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