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Published on: April 11, 2018
TNF-alpha involves in altered prefrontal synaptic transmission in mice with persistent inflammatory pain
Dong Jia1, Guo-Dong Gao, Yu Liu
1Department of Neurosurgery, Tangdu Hospital, and Department of Pharmacology, Fourth Military Medical University, Xi'an 710032, China.
Neuroscience Letters
|January 16, 2007
Summary
Tumor necrosis factor alpha (TNF-alpha) drives persistent pain by increasing in the anterior cingulate cortex (ACC). This inflammatory mediator enhances synaptic transmission, contributing to chronic pain mechanisms.
Area of Science:
- Neuroscience
- Pain Research
- Inflammation Biology
Background:
- Persistent pain involves complex neuroinflammatory processes.
- Tumor necrosis factor alpha (TNF-alpha) is linked to pain development.
- The anterior cingulate cortex (ACC) plays a role in pain modulation.
Purpose of the Study:
- Investigate TNF-alpha expression in the mouse ACC after peripheral inflammation.
- Determine the role of TNF-alpha in modulating ACC synaptic transmission.
Main Methods:
- Hind-paw administration of complete Freund's adjuvant (CFA) in mice.
- ELISA for quantifying TNF-alpha protein levels.
- In vitro whole-cell patch-clamp recordings in the ACC.
Main Results:
- CFA-induced peripheral inflammation significantly increased TNF-alpha protein levels in the ACC.
- TNF-alpha was found to enhance synaptic transmission in the ACC.
- This enhancement occurred via an increased probability of neurotransmitter release.
Conclusions:
- Peripheral inflammation up-regulates TNF-alpha expression in the ACC.
- TNF-alpha contributes to synaptic alterations in the ACC during persistent pain.
- These findings highlight TNF-alpha as a key player in ACC-mediated pain mechanisms.
