By Janet T. Spence

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Administration (Oka et al 1994b). Indeed, in keeping with the idea that IL-1 acts via prostaglandin release, prostaglandin likewise selectively exaggerates neuronal electrical activity in response to intense stimuli applied to the skin (Oka et al 1997). Although brain IL-1 can increase pain responses, spinal cord IL-1 is also key. p. administration, injection of bacterial cell walls not only induces hyperalgesia (Maier et al 1993) and increases brain IL-1 (Nguyen et al 1998; KT Nguyen, T Deak, MK Hansen, M Fleshner, LE Goehler et al, submitted for publication), it also rapidly increases IL-1 in the spinal cord dorsal horns (Watkins & Maier 1999a; KT Nguyen, T Deak, MK Hansen, M Fleshner, LE Goehler et al, submitted for publication).

As reviewed above, because all proinflammatory cytokines release IL-1, this implies that NGF is likely a common pathway to pain. -killed bacteria either to produce hyperalgesia (Poole et al 1999) or to increase NGF (Poole & Woolf 1999). Because TNF exerts at least part of its hyperalgesic actions by inducing the release of IL-1 (Poole et al 1999), it is not surprising that TNF likewise releases NGF and, in fact, acts synergistically with IL-1 to do so (Hattori et al 1993, Woolf et al 1997). Annu.

Release of proinflammatory cytokines by immune cells in the body leads, in turn, to release of proinflammatory cytokines by glia within the brain and spinal cord. Evidence is reviewed supporting the idea that proinflammatory cytokines exert powerful pain facilitatory effects following their release in the body, in the brain, and in the spinal cord. Such exaggerated pain states naturally occur in situations involving infection, inflammation, or trauma of the skin, of peripheral nerves, and of the central nervous system itself.

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