Abstract
The regulation of microRNA (miRNA) is closely related to methamphetamine (METH) addiction. Past studies have reported that miR-181a is associated with METH addiction, but the mechanism pathways remain elusive. On the basis of our past studies, which reported the endoplasmic reticulum-associated protein degradation (ERAD) mediated ubiquitin protein degradation of GABAAα1, which was involved in METH addiction. The present study, using qRT-PCR and bioinformatics analysis, further revealed that miR-181a may be indirectly responsible for the METH addiction and downregulation of GABAAα1 through the regulation of ERAD.
Highlights
Drug abuse has been widely recognized as a debilitating chronic disease of the brain, and it is one of the most dangerous diseases to human physical and mental health in modern society.Methamphetamine (METH), one of the commonly used drugs, is addictive and neurotoxic
The results indicated that the expression of miR-181a-5p (n = 8, ∗∗p < 0.01) and miR-181b-5p (n = 8, ∗p < 0.05) were downregulated in the METH-induced Conditioned Place Preference (CPP) group when compared to the control group, while the expression of miR-181c-5p and miR-181d-5p did not show any significant change (n = 8, ∗P > 0.05)
The results showed that the expression levels of 11 target genes, UBE2D3, RNF169, FBXO33, RAD23B, NEURL1B, PCNP, TULP4, KLHL15, RNF34, DERL1, HSP90B1, were upregulated in the METH-induced CPP group when compared to the control group (n = 8, P < 0.05), while the expression of 5 target genes, RNF145, KLHL5, CAND1, KLHL2, HSPA5, did not change significantly (n = 8, P > 0.05) (Figure 8)
Summary
Drug abuse has been widely recognized as a debilitating chronic disease of the brain, and it is one of the most dangerous diseases to human physical and mental health in modern society. Methamphetamine (METH), one of the commonly used drugs, is addictive and neurotoxic. Despite the severity of the consequences of drug abuse, there is still no fully effective treatment for methamphetamine addiction. Research into the mechanisms of methamphetamine addiction is critical. The neurobiology of METH is more complex than the traditional view of it as a monoaminergic modulator. It may include oxidative stress, excitatory neurotoxicity, endoplasmic reticulum stress, and neuroinflammation (Paulus and Stewart, 2020). More complex regulatory mechanisms may be involved in the addictive process of METH
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