in the extended amygdala (Kash et al., 2009). Coincidently, another miRNA, miR-9, also implicated in controlling the activity of the TLR signaling pathway through direct targeting of the NFKB1 gene in human monocytes and neutrophils (Bazzoni et al., 2009; O’Neill et al., 2011), was demonstrated to regulate ethanol sensitivity of BK channels by selectively destabilizing splice variants that contained miR-9 recognition elements, therefore making the BK channels less sensitive to alcohol (Pietrzykowski et al., 2008). We did not detect changes in miR-9 expression in our postmortem human brain study, but such differences among human alcoholics and animal models are plausible due to neurodevelopmental differences between species, stage of alcohol insult, and experimental protocol differences, to name a few. As suggested by O’Neill et al. (2011) miRNAs might also play a role in “controlling the switch from a strong early pro-inflammatory response to the resolution phase of the inflammatory process.” This would also support a case for miRNA and mRNA expression profile discrepancies depending on the stage of the inflammatory response in the particular samples under study.
