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Nociceptive and inflammatory effects of subcutaneous TNFalpha
1Department of Anesthesiology, University of California at San Diego, 9500 Gilman Drive, San Diego, USA.
Pain
|February 29, 2000
Summary
Tumor necrosis factor alpha (TNF) causes pain by sensitizing nerve fibers and increasing inflammation. This study shows TNF significantly impacts C nociceptors, contributing to hyperalgesia.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Tumor necrosis factor alpha (TNF) is a key pro-inflammatory cytokine.
- TNF contributes to pain and hyperalgesia through nerve sensitization and protein upregulation.
Purpose of the Study:
- To investigate the effects of TNF on C nociceptors and plasma extravasation in rats.
- To determine the dose-dependency and time course of TNF-induced sensitization and inflammation.
Main Methods:
- Subcutaneous injection of TNF in anesthetized rats.
- Electrophysiological recording of C nociceptor and Abeta fiber activity.
- Measurement of cutaneous plasma extravasation.
Main Results:
- TNF dose-dependently sensitized C nociceptors, lowering mechanical sensitivity and evoking ongoing activity.
- Sensitization onset was within 30 minutes and lasted over 2 hours.
- TNF increased vascular permeability in glabrous skin but did not affect Abeta fibers.
Conclusions:
- TNF plays a significant role in generating hyperalgesia and inflammation.
- The findings suggest TNF's involvement in pain and inflammation associated with disease or injury.