Abstract
Prolonged drug use causes long-lasting neuroadaptations in reward-related brain areas that contribute to addiction. Despite significant amount of research dedicated to understanding the underlying mechanisms of addiction, the molecular underpinnings remain unclear. At the same time, much of the pervasive transcription that encompasses the human genome occurs in the nervous system and contributes to its heterogeneity and complexity. Recent evidence suggests that non-coding RNAs (ncRNAs) play an important and dynamic role in transcriptional regulation, epigenetic signaling, stress response, and plasticity in the nervous system. Dysregulation of ncRNAs are thought to contribute to many, and perhaps all, neurological disorders, including addiction. Here, we review recent insights in the functional relevance of ncRNAs, including both microRNAs (miRNAs), and long non-coding RNAs, and then illustrate specific examples of ncRNA regulation in the context of drug addiction. We conclude that ncRNAs are importantly involved in the persistent neuroadaptations associated with addiction-related behaviors, and that therapies that target specific ncRNAs may represent new avenues for the treatment of drug addiction.
Highlights
Evolutionary processes in the human lineage have coupled expanding genome complexity with the acquisition, processing, and distribution of ever increasing amounts of information (Sempere et al, 2006; Mattick, 2007; Berezikov, 2011)
Chronic drug use likely perturbs these networks during the process of addiction in ways that cause a loss of plasticity and in turn establish barriers to the return to homeostasis
The complexity of the nervous system suggests that additional layers of ncRNA-mediated events likely occur during the process of addiction
Summary
Evolutionary processes in the human lineage have coupled expanding genome complexity with the acquisition, processing, and distribution of ever increasing amounts of information (Sempere et al, 2006; Mattick, 2007; Berezikov, 2011). Demonstrating a role for miRNAs in neuroplasticity, Schratt et al (2006) showed that miR-134 expression in the dendrites of developing hippocampal neurons is critically involved in dendritic spine formation and plasticity by inhibiting Lim domain-containing protein kinase 1, an important regulator of actin filament dynamics. Following this seminal report, other studies revealed that miR-138, miR-132, and miR125b play an essential role in dendritic spine formation (Siegel et al, 2009; Edbauer et al, 2010). By revealing an important miRNA-mediated epigenetic mechanism involved in drug-seeking behaviors, this study raises a number of interesting possibilities because epigenetic
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