miR-181a is a negative regulator of GRIA2 in methamphetamine-use disorder

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Abstract

A previous study reported that the miR-181a level in serum was significantly different between patients with methamphetamine-use disorder and healthy controls and that chronic methamphetamine use down-regulates the expression of miR-181a. Bioinformatic analysis predicted that miR-181a might bind the 3′-UTRs of the mRNA transcripts of the human glutamate receptor genes GRIA2 and GABRA1. In this study, we measured the expression of GRIA2 and GABRA1 in patients with methamphetamine-use disorder. In addition, we examined whether miR-181a down-regulates GRIA2 and GABRA1 in a cell-based assay. We further examined the effects of chronic methamphetamine exposure on the expression of miR-181a, GRIA2 and GABRA1. The results demonstrated that serum GRIA2 is higher in patients with methamphetamine-use disorder than in healthy controls. Dual luciferase reporter assays and a cell-based model of methamphetamine exposure also showed that miR-181a directly regulates expression of GRIA2. This study supports the evidence that miR-181a and the glutamate AMPA receptor gene GRIA2 play a critical role in methamphetamine-use disorder.

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MicroRNAs and epigenetics.

Fumiaki Sato, Soken Tsuchiya, Stephen J. Meltzer … (2011)

MicroRNAs (miRNAs) comprise species of short noncoding RNA that regulate gene expression post-transcriptionally. Recent studies have demonstrated that epigenetic mechanisms, including DNA methylation and histone modification, not only regulate the expression of protein-encoding genes, but also miRNAs, such as let-7a, miR-9, miR-34a, miR-124, miR-137, miR-148 and miR-203. Conversely, another subset of miRNAs controls the expression of important epigenetic regulators, including DNA methyltransferases, histone deacetylases and polycomb group genes. This complicated network of feedback between miRNAs and epigenetic pathways appears to form an epigenetics-miRNA regulatory circuit, and to organize the whole gene expression profile. When this regulatory circuit is disrupted, normal physiological functions are interfered with, contributing to various disease processes. The present minireview details recent discoveries involving the epigenetics-miRNA regulatory circuit, suggesting possible biological insights into gene-regulatory mechanisms that may underlie a variety of diseases. © 2011 The Authors Journal compilation © 2011 FEBS.

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Formation of accumbens GluR2-lacking AMPA receptors mediates incubation of cocaine craving.

Kelly Conrad, Kuei Tseng, Jamie Uejima … (2008)

Relapse to cocaine use after prolonged abstinence is an important clinical problem. This relapse is often induced by exposure to cues associated with cocaine use. To account for the persistent propensity for relapse, it has been suggested that cue-induced cocaine craving increases over the first several weeks of abstinence and remains high for extended periods. We and others identified an analogous phenomenon in rats that was termed 'incubation of cocaine craving': time-dependent increases in cue-induced cocaine-seeking over the first months after withdrawal from self-administered cocaine. Cocaine-seeking requires the activation of glutamate projections that excite receptors for alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) in the nucleus accumbens. Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from cocaine self-administration by the addition of new AMPA receptors lacking glutamate receptor 2 (GluR2). Furthermore, we show that these new receptors mediate the incubation of cocaine craving. Our results indicate that GluR2-lacking AMPA receptors could be a new target for drug development for the treatment of cocaine addiction. We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of GluR2-lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine-related cues, leading to an intensification of drug craving and relapse.

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MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212

Heh-In Im, Jonathan Hollander, Purva Bali … (2010)

The X-linked transcriptional repressor methyl CpG binding protein 2 (MeCP2), known for its role in the neurodevelopmental disorder Rett syndrome, is emerging as an important regulator of neuroplasticity in post-mitotic neurons. Cocaine addiction is commonly viewed as a disorder of neuroplasticity, but the potential involvement of MeCP2 has not been explored. Here we identify a key role for MeCP2 in the dorsal striatum in the escalating cocaine intake seen in rats with extended access to the drug, a process that mimics the increasingly uncontrolled cocaine use seen in human addicts. MeCP2 regulates cocaine intake through homeostatic interactions with microRNA-212 (miR-212) to control the effects of cocaine on striatal brain-derived neurotrophic factor (BDNF) levels. These data suggest that homeostatic interactions between MeCP2 and miR-212 in dorsal striatum may play an important role in regulating vulnerability to cocaine addiction.

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Journal

Journal ID (nlm-ta): Sci Rep

Journal ID (iso-abbrev): Sci Rep

Title: Scientific Reports

Publisher: Nature Publishing Group

ISSN (Electronic): 2045-2322

Publication date (Electronic): 21 October 2016

Publication date Collection: 2016

Volume: 6

Electronic Location Identifier: 35691

Affiliations

[1 ]Collaborative Innovation Center for Brain Science, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine , 600 Wan Ping Nan Road, Shanghai 200030, China

[2 ]Wuxi Mental Health Center, Nanjing Medical University , 156 Qian Rong Road, Wuxi 214151, China

[3 ]Shanghai Key Laboratory of Psychotic Disorders , Shanghai, PR China

[4 ]Brain Science and Technology Research Center, Shanghai Jiao Tong University Shanghai , PR China

Author notes

[a ] yushuny@ 123456yahoo.com

[b ] drminzhao@ 123456gmail.com

[*]

These authors contributed equally to this work.

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Publisher Item ID: srep35691

DOI: 10.1038/srep35691

PMC ID: 5073328

PubMed ID: 27767084

SO-VID: 06baca34-6089-4187-8033-7c7e359f883b

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miR-181a is a negative regulator of GRIA2 in methamphetamine-use disorder

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Most cited references 26

MicroRNAs and epigenetics.

Formation of accumbens GluR2-lacking AMPA receptors mediates incubation of cocaine craving.

MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212

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