Studies of the effects of alcohol on miRNA expression suggest that miRNAs work in coordinated fashion to promote drug adaptation and neuronal plasticity and that this may occur in a relatively rapid fashion. For example, miR-9 is expected to mediate alcohol-related post-transcriptional regulation of neuronal BK mRNA and can do so rapidly upon exposure (Pietrzykowski et al., 2008; Treistman & Martin, 2009). More specifically, mRNA encoding the voltage-gated potassium channel (BK) is decreased within 15 minutes of exposing rat striatal cultures to alcohol. BK influences the the control of alcohol intake and tolerance in an individual. This decrease in BK mRNA resulted from increased miR-9 expression and downstream degredation of BK splice variants containing a miR-9 binding site in their 3′UTR. The remaining BK variants were those least affected by the presence of alcohol. In addition to changes in BK expression, miR-9 targets several other genes that influence alcohol use (e.g., neuronal exitability- GABRB2 and DRD2, function of presynaptic terminals- GABRB2, and gene expression and lipid metabolism- PPARA, peroxisome proliferator-activated receptor alpha). Rat studies suggest that other families of miRNAs
