By Janet T. Spence
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Extra resources for Annual Review of Psychology, vol 51 2000
IL-1 actions have been variously argued to (a) reflect direct IL-1 binding and activation of sensory nerves, (b) be dependent on the release of prostaglandins that sensitize pain fibers (Ferreira 1972), (c) work via pathways that are independent of prostaglandins, or (d) be dependent on the release of NGF (Poole et al 1999, Poole & Woolf 1999). All four mechanisms actually do appear to mediate IL-1 actions to varying degrees, depending on the exact circumstances under study (Poole et al 1999, Poole & Woolf 1999).
However, from the work reviewed above, this is clearly an issue that warrants serious consideration. In AIDS, as the example, upwards of 80% of patients suffer from chronic pain, and of these, a shockingly high percentage suffer from vague and diffuse pains of unknown origin (Breitbart et al 1996, Hewitt et al 1997). Clearly, AIDS patients suffer from pain from a variety of readily identifiable causes, including nerve damage, opportunistic cancers, and opportunistic infections, resulting both from the drugs used in therapy and from the disease process itself (Breitbart et al 1996, Hewitt et al 1997).
Simply injecting TNF onto the sensory nerve both elicits hyperalgesia and allodynia (Wagner & Myers 1996a) and directly activates peripheral nerves that normally respond only to painful stimuli in the skin (Sorkin et al 1997). As noted above for Aplysia (Clatworthy 1999), it has been proposed that hyperexcitability induced by TNF results directly from alterations of ion channels in the sensory neuron (Baldwin et al 1996, Kagan et al 1992). Placing killed bacteria (Clatworthy et al 1995, Eliav et al 1996), viral coat proteins (Herzberg et al 1998), algae protein (Eliav et al 1996), or a foreign body such as chromic gut surgical sutures (Maves et al 1993) near sensory Annu.
Annual Review of Psychology, vol 51 2000 by Janet T. Spence