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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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Related Experiment Video

Updated: Jul 26, 2025

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
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Non-Coding RNAs Regulate Spinal Cord Injury-Related Neuropathic Pain via Neuroinflammation.

Jing Zhu1, Fei Huang1,2, Yonglin Hu1,3

  • 1Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, JiangSu Province, 226001, People's Republic of China.

Journal of Inflammation Research
|June 19, 2023
PubMed
Summary
This summary is machine-generated.

Spinal cord injury (SCI) can cause chronic neuropathic pain (NP) and dysfunction. Non-coding RNAs (ncRNAs) show promise in reducing neuroinflammation and improving NP outcomes after SCI.

Keywords:
neuroinflammationneuropathic painnon‐coding RNAsspinal cord injury

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Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Spinal cord injury (SCI) frequently results in chronic neuropathic pain (NP) and significant quality of life reduction.
  • The inflammatory response post-SCI is a key factor in the development and progression of NP.
  • Current treatment strategies for SCI-related NP face challenges due to complex underlying mechanisms.

Purpose of the Study:

  • To investigate the role of non-coding RNAs (ncRNAs) in the context of SCI-induced neuropathic pain.
  • To explore how ncRNAs modulate neuroinflammation and gene expression following SCI.
  • To assess the potential of targeting ncRNAs for improved NP prognosis in SCI patients.

Main Methods:

  • Review of existing clinical trials and experimental models of SCI-related NP.
  • Analysis of studies focusing on the molecular mechanisms of ncRNAs in SCI.
  • Examination of ncRNA interactions with target messenger RNAs (mRNAs) and immunocytes.

Main Results:

  • Neuroinflammation is a critical mediator in the development of NP after SCI.
  • Non-coding RNAs (ncRNAs) have been identified as key regulators of gene expression in SCI.
  • ncRNAs can interact with glia, neurons, and immunocytes to modulate inflammatory responses.

Conclusions:

  • Reducing neuroinflammation following SCI may alleviate NP symptoms.
  • Non-coding RNAs (ncRNAs) play a significant role in regulating inflammation and gene expression post-SCI.
  • Targeting ncRNAs presents a potential therapeutic avenue for managing neuropathic pain in spinal cord injury patients.