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Neuroscience letters · Jan 2002
Capsaicin sensitive afferents mediate the development of heat hyperalgesia and hindpaw edema after sciatic section in rats.
- Wade S Kingery, Geeta S Agashe, Tian Zhi Guo, M Frances Davies, J David Clark, and Mervyn Maze.
- Department of Functional Restoration, Stanford University School of Medicine, Stanford, CA, USA. wkingery@stanford.edu
- Neurosci. Lett. 2002 Jan 18; 318 (1): 39-43.
AbstractSciatic section in rats evokes chronic hyperalgesia, autotomy pain behavior, and hindpaw edema, a constellation resembling complex regional pain syndrome (CRPS) in man. Glucocorticoid treatment inhibits these sequelae of sciatic section and also blocks neurogenic extravasation. Small diameter afferent neurons release substance P (SP), a mediator of both hyperalgesia and neurogenic extravasation. Now, we show that pre-emptive destruction of the small diameter fibers prevents neurogenic extravasation, and prevented the development of heat hyperalgesia and hindpaw edema after sciatic section. Thus, capsaicin sensitive primary afferent neurons which release SP are required for the development of heat hyperalgesia and hindpaw edema in this animal model of CRPS.
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