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Analgesia and Pain Management01:25

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Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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Opioids are a class of drugs that mimic endogenous opioid peptides and act on opioid receptors, and help in pain relief. These compounds are classified as natural, synthetic, or semi-synthetic. Natural opioids, like morphine, codeine, and thebaine, are derived from the opium poppy plant (Papaver somniferum or Papaver album) and are termed opiates. Synthetic opioids are artificial, while semi-synthetic opioids combine natural and synthetic compounds. Morphine, a prototypical opioid, possesses a...
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Opioid Receptors: Overview01:22

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Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2,...
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Synthetic and semisynthetic opioids are pivotal in pain management and tackling opioid addiction. Semisynthetic opioids, including morphinans (morphine derivatives), oxycodone, oxymorphone, hydrocodone, and hydromorphone, have improved pharmacokinetic profiles compared to morphine. Additionally, heroin and 6-MAM (6-Monoacetylmorphine) show better CNS penetration than morphine due to heightened lipid solubility. Hydromorphone, a potent opioid, undergoes hepatic metabolism to form the active...
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Related Experiment Video

Updated: May 23, 2025

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
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Morphine-induced hyperalgesia impacts small extracellular vesicle microRNA composition and function.

Deepa Reddy1, Zhucheng Lin1, Sujay Ramanathan1

  • 1Department of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.

The Journal of Pharmacology and Experimental Therapeutics
|March 7, 2025
PubMed
Summary
This summary is machine-generated.

Chronic morphine alters serum small extracellular vesicles (sEVs) microRNA in mice. These sEVs, containing specific microRNAs, can reduce pain hypersensitivity, suggesting a potential non-opioid pain therapy.

Keywords:
CREBMicroRNAMorphineOpioid-induced hyperalgesiaSmall extracellular vesicles

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Opioid analgesics like morphine are widely used for pain management.
  • Prolonged opioid use can paradoxically increase pain sensitivity, a phenomenon known as opioid-induced hyperalgesia.
  • The molecular mechanisms driving opioid-induced hyperalgesia remain incompletely understood.

Purpose of the Study:

  • To investigate molecular changes in serum small extracellular vesicles (sEVs) following morphine treatment that induces hyperalgesia.
  • To identify specific microRNAs (miRNAs) within sEVs that may regulate pain pathways.
  • To assess the therapeutic potential of morphine-altered sEVs in modulating pain sensitivity.

Main Methods:

  • Induction of hyperalgesia in mice using a morphine treatment paradigm.
  • Analysis of miRNA composition in serum-derived sEVs from treated and control mice.
  • Bioinformatic prediction and experimental validation of miRNA targets, including CREB (cyclic AMP response element binding protein).
  • Administration of sEVs to naïve recipient mice to assess their impact on nociceptive behavior.

Main Results:

  • Significant differential expression of 18 miRNAs was observed in sEVs from morphine-treated mice.
  • miR-155 and miR-10a within sEVs were confirmed to bind and repress Creb mRNA.
  • Intrathecal injection of sEVs did not alter basal pain thresholds but accelerated the resolution of inflammatory hypersensitivity in recipient mice.
  • Administration of these sEVs did not affect other behaviors like conditioned place preference or locomotor sensitization.

Conclusions:

  • Morphine treatment alters the miRNA cargo of serum sEVs.
  • These sEVs, particularly those modulating CREB expression, show potential for treating pain hypersensitivity.
  • Serum sEVs represent a promising non-opioid therapeutic strategy for pain management and offer insights into opioid-induced hyperalgesia pathophysiology.