Conversely, as our understanding of the neurobiology of addiction improves, we have novel candidate genetic targets to consider. One such example are microRNAs (miRNA) that interact with the 3′-untranslated region (3′-UTR) of the target mRNA and can mediate their degradation or repress translation (13). Upon development of drug dependence, the brain undergoes significant remodeling and adaptation, and the expression profile of a number of genes in the brain are known to change following acute and repeated administration of psychostimulants and other drugs of abuse (14). These changes are thought to represent a compensatory mechanism to maintain homeostasis in response to drug-induced effects, and are manifested as drug-seeking behaviors, withdrawal and tendency to relapse. With the discovery of miRNAs and their role in the regulation of gene expression it has been proposed that drug-induced gene expression changes may be mediated through this intermediate pathway. One study has shown that nicotine treatment up- and down-regulates a number of miRNAs, in particular miR-140*, which regulates the expression of a number of genes including dynamin 1 (Dmn1) that may be involved in endocytosis and
