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Related Concept Videos

Nociception01:44

Nociception

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. Thus, pain helps the...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Analgesia and Pain Management01:25

Analgesia and Pain Management

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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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Pain01:20

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Related Experiment Video

Updated: Jul 27, 2026

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
07:09

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Published on: July 16, 2014

Brain-derived TNFalpha mediates neuropathic pain.

T A Ignatowski1, W C Covey, P R Knight

  • 1Department of Pathology, State University of New York at Buffalo, 14214, USA.

Brain Research
|November 5, 1999
PubMed
Summary

Brain-derived tumor necrosis factor (TNF) plays a key role in neuropathic pain. Blocking TNF in the brain reduces pain hypersensitivity, suggesting a central role for TNF in pain perception.

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Last Updated: Jul 27, 2026

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice
07:09

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Published on: July 16, 2014

Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice
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Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies
08:16

Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies

Published on: October 6, 2022

Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Neuropathic pain involves central mechanisms following nerve injury, but these are not fully understood.
  • Tumor necrosis factor (TNF) is implicated in pain pathways.
  • The role of brain-associated TNF in neuropathic pain requires further investigation.

Purpose of the Study:

  • To investigate the role of brain-associated TNF in the development of hyperalgesia in the chronic constriction injury (CCI) model of neuropathic pain.
  • To assess the impact of TNF modulation in the brain on pain perception and hippocampal noradrenergic neurotransmission.

Main Methods:

  • Rats underwent sciatic nerve ligation (CCI model) to induce neuropathic pain.
  • TNF levels in brain, spinal cord, and plasma were measured.
  • Intracerebroventricular (i.c.v.) microinfusion of TNF-antibodies or recombinant TNF-alpha was administered.

Main Results:

  • Bioactive TNF levels were elevated in the hippocampus following CCI.
  • Hippocampal TNF elevation correlated with decreased norepinephrine release.
  • i.c.v. infusion of TNF-antibodies abolished hyperalgesia when started early post-injury.
  • i.c.v. infusion of TNF-alpha exacerbated hyperalgesia and decreased hippocampal adrenergic neurotransmission.

Conclusions:

  • Brain-derived TNF is crucial in the pathology of neuropathic pain.
  • Central TNF signaling contributes to pain hypersensitivity and altered neurotransmission.
  • Targeting brain TNF may offer a therapeutic strategy for neuropathic pain.