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Corticotropin-releasing factor in antinociception and inflammation
M Schäfer1, S A Mousa, C Stein
1Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse, NIH, Baltimore, MD 21224, USA. m.schaefer@lrz.uni-muenchen.de
European Journal of Pharmacology
|March 26, 1997
Summary
Corticotropin-releasing factor (CRF) in peripheral tissues modulates inflammatory pain by triggering local opioid release. This conserved mechanism helps maintain bodily homeostasis during stress.
Area of Science:
- Neuroendocrinology
- Immunology
- Pain Research
Background:
- Corticotropin-releasing factor (CRF) is crucial for central stress responses.
- CRF's role in peripheral tissues, particularly in pain and inflammation, is increasingly recognized.
- CRF and its receptors are upregulated in inflammatory pain conditions.
Purpose of the Study:
- To investigate the role of peripherally expressed CRF in inflammatory pain.
- To elucidate the mechanism by which local CRF influences pain transmission.
- To explore the evolutionary conservation of CRF-like peptides and stress responses.
Main Methods:
- Analysis of CRF and receptor expression in inflammatory pain states.
- Investigation of local CRF actions on immune cells and sensory nerves.
- Comparative analysis of CRF-like peptides across species.
Main Results:
- Locally expressed CRF acts on immune cells expressing CRF receptors.
- This interaction induces the release of opioid peptides from immune cells.
- These opioids inhibit peripheral sensory nerve transmission, reducing pain.
Conclusions:
- Peripheral CRF plays a significant role in modulating inflammatory pain via a paracrine mechanism.
- This pathway involves immune cell-mediated opioid release, acting on peripheral nerves.
- The conserved nature of CRF-like peptides suggests an ancient stress-response system.