• Pain · Mar 2017

    A mouse model for chronic pain-induced increase in ethanol consumption.

    • Ryan K Butler, Darin J Knapp, Veronica Ulici, Lara Longobardi, Richard F Loeser, and George R Breese.
    • aBowles Center for Alcohol Studies, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA bDepartment of Psychiatry, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA cThurston Arthritis Research Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA dDivision of Rheumatology, Allergy and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, Department of Medicine eDepartment of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA fCurriculum in Neurobiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA gThe UNC Neuroscience Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    • Pain. 2017 Mar 1; 158 (3): 457-462.

    AbstractChronic pain conditions are often comorbid with alcohol abuse. "Self-medication" with alcohol introduces a host of problems associated with the abuse of alcohol which over time has the potential of exacerbating the painful condition. Despite the prevalence of chronic pain being associated with alcohol abuse, rodent models which mimic the comorbid conditions are lacking. In this study, we model osteoarthritis (OA) in C57BL/6J mice by surgically destabilizing the medial meniscus (DMM). Sham-operated mice served as controls. Thirteen weeks after surgery, DMM but not sham-operated mice exhibited pronounced incapacitance of the surgically manipulated hind limb compared with the nonsurgically manipulated hind limb. At this time, the mice were exposed to the 2-bottle ethanol choice, beginning with 2.5% with a gradual increasing to 20%. Compared with sham controls, DMM mice consumed more EtOH and preferred EtOH over water at the 20% EtOH concentration. Histological analysis verified that the DMM mice exhibited significant damage to the articular cartilage and osteophyte growth compared with sham controls and these measures of the severity of OA correlated with the amount of ethanol intake. Thus, the combination of the DMM model of OA with the enhanced two-bottle ethanol choice is a potential preclinical approach in mice by which the basis of the comorbid association of alcohol abuse and chronic pain conditions can be explored.

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