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Related Concept Videos

Nociception01:44

Nociception

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Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
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Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

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Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
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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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Related Experiment Video

Updated: Mar 30, 2026

Tissue Preparation and Immunostaining of Mouse Sensory Nerve Fibers Innervating Skin and Limb Bones
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DNA Methylation Modulates Nociceptive Sensitization after Incision.

Yuan Sun1,2, Peyman Sahbaie1,2, DeYong Liang1,2

  • 1Department of Anesthesiology, Stanford University School of Medicine, Stanford, California, United States of America.

Plos One
|November 5, 2015
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Summary

DNA methylation influences postoperative pain by altering opioid receptor expression. Inhibiting DNA methylation reduced pain sensitivity and inflammation, highlighting a potential therapeutic target for incisional pain management.

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Area of Science:

  • Epigenetics
  • Pain research
  • Neuroscience

Background:

  • DNA methylation is a crucial epigenetic regulator of gene expression and DNA accessibility.
  • While its role in neuropathic and inflammatory pain is known, its involvement in postoperative pain remains unexplored.
  • Investigating DNA methylation's role in incisional pain is essential for understanding and managing surgical pain.

Purpose of the Study:

  • To explore the role of DNA methylation in modulating incisional pain.
  • To identify potential DNA methylation targets involved in incisional pain.
  • To elucidate the mechanisms underlying DNA methylation's effect on postoperative pain.

Main Methods:

  • Utilized the DNA methyltransferase (DNMT) inhibitor 5-Aza-2'-deoxycytidine to assess its impact on pain behaviors.
  • Measured mechanical allodynia, thermal sensitivity, and hindpaw swelling in an incisional pain model.
  • Analyzed global DNA methylation and DNMT expression in skin, spinal cord, and dorsal root ganglia (DRG).
  • Examined the expression of proopiomelanocortin (Pomc) and Oprm1 (mu-opioid receptor).
  • Investigated the effect of the opioid receptor antagonist naloxone on incision-induced hypersensitivity.

Main Results:

  • 5-Aza-2'-deoxycytidine significantly reduced mechanical allodynia, thermal sensitivity, and hindpaw swelling, indicating anti-allodynic and anti-inflammatory effects.
  • Incisional injury increased global DNA methylation and DNMT3b expression in the skin, but not in the spinal cord or DRG.
  • Peripheral expression of Pomc and Oprm1 was upregulated post-incision, with Oprm1 further increased by DNMT inhibitor treatment.
  • Naloxone administration exacerbated incision-induced mechanical hypersensitivity, confirming the role of opioid receptors.

Conclusions:

  • DNA methylation is functionally implicated in incisional nociceptive sensitization.
  • Mu-opioid receptor signaling represents a key pathway regulated by DNA methylation in controlling postoperative pain sensitization.
  • Targeting DNA methylation pathways offers a potential strategy for managing incisional pain.