期刊
PAIN
卷 85, 期 1-2, 页码 145-151出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/S0304-3959(99)00262-6
关键词
neuropathic pain; receptor sensitization; electrophysiology
资金
- NINDS NIH HHS [NS 35630] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS035630] Funding Source: NIH RePORTER
Tumor necrosis factor alpha (TNF) is a potent pro-inflammatory cytokine that produces pain and hyperalgesia following injection. Its algesic effects are due to sensitizing actions on nociceptive primary afferents and to the upregulation of other pro-inflammatory and algesic proteins. In anesthetized rats, we investigated the effect of subcutaneously injected TNF on background activity and mechanical sensitivity of C nociceptors of the sural nerve, as well as its effects on cutaneous plasma extravasation. TNF sensitized C nociceptors dose-dependently; the optimal dose (5 ng) lowered threshold in 66.7% of the tested fibers. This sensitization occurred within 30 min and could last for 2 or more hours. Injected TNF had no effect on A beta mechanoreceptive fibers. In addition, TNF evoked ongoing activity in 14% of C nociceptors and caused significant and dose-related increases in vascular permeability in glabrous skin. Our data suggest that TNF released during disease or after tissue injury participates in the generation of hyperalgesia and inflammation. (C) 2000 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.
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