The family miR-148/152 was recently reported to inhibit TLR-triggered MHCII expression and functional maturation of dendritic cells (DCs). By targeting CaMKIIα, miR-152 inhibited the production of cytokines, including IL12, IL6, TNFα, and IFNβ, and negatively regulated the innate response (Liu et al., 2010). Coincidently, miR-152 was also upregulated in fetal brain from mice exposed to ethanol during gestation (Wang et al., 2009). Interestingly, Kash et al. (2009) recently found a significant decrease in the total levels of CaMKIIα in the central extended amygdala after ethanol exposure in mice. CaMKIIα expression enhances the extent of desensitization of NR2B-containing NMDA receptors in heterologous cells (Sessoms-Sikes et al., 2005) and regulates ethanol sensitivity of BK channels (Liu et al., 2006a), which suggested the possibility that reduced levels of CaMKIIα could be acting in a general fashion to modulate the ethanol sensitivity of channels 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
