Figure 7.
Model for COX-1- and COX-2-derived PGs in inflammation and pain. The initial peripheral inflammatory signal causes local upregulation of COX-2 and PGs that mediate plasma extravasation and neurological signals to the CNS. Inflammatory mediators including PGs increase nerve traffic, resulting in increased COX-2 expression in the spinal cord, which in turn produces PGs that influence central pain signals.