to translation repression without affecting the mRNA levels. A similar mechanism for repression of translational initiation of let-7 targets in human cells had previously been reported (Pillai, 2005). The μ opioid receptor is largely distributed along reward circuits, where it mediates the reinforcing activities of morphine and several non-opioid drugs such as alcohol, cannabinoids, and nicotine. The non-opioid drugs act at their own receptors [GABAA and NMDA receptors for alcohol, CB1 and CB2 receptors for cannabinoids, and nicotinic acetylcholine receptor (nAChR) for nicotine] and are likely to induce the release of endogenous opioid peptides that, in turn, activate the μ receptors. This type of receptor seems to function as a convergent molecular gate in the initiation of addictive behaviors (Contet et al., 2004). In addition, Wang et al. (2011) demonstrated that let-7f targeted β2-adrenergic receptor (β2AR) mRNA and repressed expression of the native ADRB2 protein in the human cell line H292. Interestingly, another microRNA that is also upregulated in human alcoholics, miR-15, belongs to one of the only two other groups of miRNAs that have predicted binding sites within the 3′ UTR of the β2AR mRNA (Wang et al., 2011). Recent evidence supports a role for β-adrenergic receptors in retrieval
