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Alternative Splicing Mechanisms Underlying Opioid-Induced Hyperalgesia. | LitMetric

AI Article Synopsis

  • Prolonged opioid use can lead to a condition called opioid-induced hyperalgesia (OIH), where the pain sensitivity increases instead of decreases.
  • A study investigated the role of alternative splicing in genes and how they contribute to OIH, revealing different patterns of gene expression in certain brain regions of mice exposed to chronic morphine.
  • The findings emphasize the importance of understanding specific gene isoforms and regulatory factors involved in OIH to better comprehend the effects of morphine on pain sensitivity.

Article Abstract

Prolonged use of opioids can cause opioid-induced hyperalgesia (OIH). The impact of alternative splicing on OIH remains partially characterized. A study of the absolute and relative modes of action of alternative splicing further the understanding of the molecular mechanisms underlying OIH. Differential absolute and relative isoform profiles were detected in the trigeminal ganglia and nucleus accumbens of mice presenting OIH behaviors elicited by chronic morphine administration relative to control mice. Genes that participate in glutamatergic synapse (e.g., Grip1, Grin1, Wnk3), myelin protein processes (e.g., Mbp, Mpz), and axon guidance presented absolute and relative splicing associated with OIH. Splicing of genes in the gonadotropin-releasing hormone receptor pathway was detected in the nucleus accumbens while splicing in the vascular endothelial growth factor, endogenous cannabinoid signaling, circadian clock system, and metabotropic glutamate receptor pathways was detected in the trigeminal ganglia. A notable finding was the prevalence of alternatively spliced transcription factors and regulators (e.g., Ciart, Ablim2, Pbx1, Arntl2) in the trigeminal ganglia. Insights into the nociceptive and antinociceptive modulatory action of Hnrnpk were gained. The results from our study highlight the impact of alternative splicing and transcriptional regulators on OIH and expose the need for isoform-level research to advance the understanding of morphine-associated hyperalgesia.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8535871PMC
http://dx.doi.org/10.3390/genes12101570DOI Listing

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