Brain, behavior, and immunity
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Brain Behav. Immun. · Oct 2008
Contribution of activated interleukin receptors in trigeminal ganglion neurons to hyperalgesia via satellite glial interleukin-1beta paracrine mechanism.
The present study investigated whether under in vivo conditions, inflammation alters the excitability of nociceptive Adelta-trigeminal ganglion (TRG) neurons innervating the facial skin via a cytokine paracrine mechanism. We used extracellular electrophysiological recording with multibarrel-electrodes in this study, and complete Freund's adjuvant (CFA) was injected into the rat facial skin. The threshold for escape from mechanical stimulation applied to the whisker pad area in inflamed rats (2 days after CFA injection) was significantly lower than that in control rats. ⋯ The mechanical threshold of nociceptive-TRG neurons in inflamed rats was significantly lower than that in control rats, but was not significantly different between control and inflamed rats after application of an IL-1ra. These results suggested that inflammation modulates the excitability of nociceptive Adelta-TRG neurons innervating the facial skin via IL-1beta paracrine action within trigeminal ganglia. Such an IL-1beta release could be important in determining trigeminal inflammatory hyperalgesia.
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Brain Behav. Immun. · Oct 2008
Interleukin-1 signaling is required for induction and maintenance of postoperative incisional pain: genetic and pharmacological studies in mice.
Postoperative incisional pain is characterized by persistent acute pain in the area of the cut, and is associated with release of proinflammatory cytokines, including interleukin-1 (IL-1), which play important hyperalgesic and allodynic roles in various inflammatory conditions. In the present study, we tested the role of IL-1 signaling in postoperative incisional pain using three mouse strains impaired in IL-1 signaling due to deletion of the IL-1 type I receptor on a mixed genetic background (IL-1rKO) or congenic background (IL-1rKOCog), or due to transgenic over-expression of IL-1 receptor antagonist (IL-1raTG). We used the relevant wild-type (WT) mice both as controls for the mutant strains, and for assessing the effects of pharmacological blockade of IL-1-signaling. ⋯ To test the hypothesis that IL-1-signaling is also involved in the maintenance of postoperative pain, WT mice were acutely treated with IL-1ra 24h following the incision, when allodynia was already evident. This treatment reversed the allodynic response throughout the observation period. Together, these findings suggest that IL-1 plays a critical role in the development and maintenance of postoperative incisional pain.