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Related Concept Videos

Nociception01:44

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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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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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Pain serves as a critical warning signal that alerts the body to potential or actual harm. When mechanical pressure on the skin is intense, such as from a sharp pinch, the sensation transitions from touch to pain. Similarly, extreme temperatures, like a hot pot handle, convert the sensation of heat into pain. Pain can also result from overstimulation of other senses, such as blinding light, loud noise, or the intense heat from habañero peppers. This ability to sense pain is essential for...
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Spinal-Specific Super Enhancer in Neuropathic Pain.

Yang Tao1, Qi-Hui Wang1, Xiao-Tong Li1

  • 1Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Xuzhou Medical University, Xuzhou 221004, China.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|October 6, 2023
PubMed
Summary
This summary is machine-generated.

Super enhancers (SEs) drive neuropathic pain by regulating Ntmt1 and Prrx2 gene expression in spinal cord neurons. Inhibiting bromodomain-containing protein 4 (BRD4) or deleting SEs alleviates pain, highlighting BRD4 inhibitors as a potential therapy.

Keywords:
BRD4 inhibitorNtmt1Prrx2neuropathic painsuper enhancer

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Dysfunctional gene expression in nociceptive pathways is key to neuropathic pain.
  • Super enhancers (SEs) regulate gene expression, but their role in pain is unknown.

Purpose of the Study:

  • To investigate the role of SEs in chronic constriction injury (CCI)-induced neuropathic pain.
  • To identify specific SEs and their target genes involved in pain signaling.

Main Methods:

  • Identified a spinal-specific SE (SS-SE) regulating Ntmt1 and Prrx2 in dorsal horn neurons.
  • Utilized bromodomain-containing protein 4 (BRD4) inhibition (JQ1) and CRISPR-Cas9 for SE deletion.
  • Assessed gene expression (NTMT1, PRRX2, p-ERK, GFAP) and pain behaviors in mouse models.

Main Results:

  • CCI enhanced SS-SE activity and NTMT1/PRRX2 expression in a BRD4-dependent manner.
  • BRD4 inhibition and SS-SE deletion attenuated hypersensitivity and normalized gene expression.
  • Knockdown of Ntmt1 or Prrx2, or their mimicry in naive mice, altered pain behaviors.

Conclusions:

  • BRD4-driven SS-SE activity in dorsal horn neurons drives neuropathic pain via Ntmt1/Prrx2.
  • Targeting SS-SE or BRD4 offers a novel therapeutic strategy for neuropathic pain.
  • This study redefines understanding of pain-related gene regulation.