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By Janet T. Spence

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Extra info for Annual Review of Psychology, vol 51 2000

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The brain expresses receptors for IL-1, and blocking IL-1 actions in the brain blocks sickness responses (Maier & Watkins 1998, Rothwell & Luheshi 1994). To summarize, infection/injury in the body leads to the activation of immune cells. In the early stages of this immune response, a variety of substances, including proin- CYTOKINES AND PAIN 39 flammatory cytokines (TNF, IL-1, IL-6), are released at the infection/injury site. For abdominal immune activation at least, this may trigger the activation of sensory paraganglia that communicate to sensory nerves in the vagus.

The general term hyperalgesia is most accurately subdivided into two forms: hyperalgesia and allodynia (Willis 1992). Hyperalgesia, as used here, refers to a lowering of pain threshold such that stimuli that were not originally painful now are. Hyperalgesia is typically assessed in the laboratory using radiant heat stimuli. In the studies cited in this review, thermal hyperalgesia is almost always the form assessed. Hyperalgesia involves a ‘‘plastic’’ change in the spinal cord dorsal horn response (Liu & Sandkuhler 1998, Sandkuhler & Liu 1998), similar if not identical to the long-term potentiation (LTP) that some believe underlies learning and memory in the Annu.

For personal use only. 48 WATKINS Ⅲ MAIER of drugs that disrupt glial function or specific glial mediators yet been tested. Furthermore, spinal cord trauma recruits immune cells from the general circulation into the region (Carlson et al 1998, Popovich et al 1997), activates both astrocytes (Hadley & Goshgarian 1997) and microglia (Popovich et al 1997), and causes exaggerated pain states in both laboratory animals and humans (Christensen & Hulsebosch 1997, Wang et al 1997, Xu et al 1993). The potential role of glia and proinflammatory cytokines in these pain states has yet to be explored.

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