Rodent models of human alcoholism: implications for a role of neuropeptide Y and corticotropin releasing factor Public Deposited
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- Last Modified
- March 21, 2019
Sparta, Dennis R.
- Affiliation: College of Arts and Sciences, Department of Psychology and Neuroscience
- Rodent models of alcoholism have been integral in discovering candidate genes and neurochemicals involved in this disease. Two promising candidates include neuropeptide Y (NPY) and corticotropin releasing factor (CRF). It has been hypothesized that NPY and CRF exert a reciprocal regulation of ethanol self-administration through allosteric interactions within the extended amygdala. Therefore, the goal of the present report was to determine if NPY and CRF modulate ethanol relapse- and binge-like drinking behaviors through the use of recently developed rodent models. Experiment 1 utilized the NPY -/- mouse to determine if NPY modulates withdrawal-induced anxiety, a component of ethanol relapse. Compared to the NPY +/+ mice, NPY -/- mice exhibited increased withdrawal-induced anxiety as measured by the elevated plus maze (EPM) test. Although, we did not examine CRF, previous research has revealed that a hyperactive CRF system contributes to withdrawal-induced anxiety. Experiment 2 expanded on previous findings by examining the role of NPY and CRF on excessive ethanol relapse-like consumption, as measured by the alcohol deprivation effect (ADE). We found that female NPY -/- mice exhibited increased post-deprivation ethanol drinking (i.e., the ADE) that endured for several deprivation cycles. Interestingly, the male NPY -/- mice did not exhibit the ADE during any deprivation cycle. Additionally, we found that acute administration of CP-154,526, a highly selective CRF1 receptor antagonist, reduced the expression of the ADE in mice. Experiment 3 examined the role of CRF on excessive or binge-like drinking as modeled by drinking in the dark (DID) procedures. We found that administration of CP-154,526 reduced excessive, but not moderate, ethanol drinking suggesting a possible role for CRF in binge drinking. Taken together, these experiments provide evidence for a role of both NPY and CRF in the modulation of multiple behaviors and neurobiological responses that may underlie alcohol abuse disorders and alcoholism. Ultimately, pharmacological compounds that target these systems may be of potential therapeutic value for the treatment of alcoholism.
- Date of publication
- December 2007
- Resource type
- Rights statement
- In Copyright
- Thiele, Todd
- Degree granting institution
- University of North Carolina at Chapel Hill
- Open access
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|Rodent models of human alcoholism : implications for a role of neuropeptide Y and corticotropin releasing factor||2019-04-10||Public||