Interestingly, previous behavioral studies by Blednov et al. have shown that CCR2-knockout mice have reduced preference and consumption of ethanol, while CCR5-knockout mice increase their consumption and preference compared with wild-type mice [5]. CVC acts as a dual inhibitor blocking both the CCR2 and CCR5 receptors. Therefore, our observation of no change in consumption or preference in CVC-treated mice may be explained by the previous observations that CCR2 and CCR5 genetic deficiencies have opposite effects on alcohol use or preference. Using a dual inhibitor, we may have negated any effect on ethanol-seeking behavior and thus isolated a direct biologic effect of the CVC molecule on the underlying biologic pathology associated with alcohol use rather than influencing behavior and ethanol exposure.
