By Janet T. Spence
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Additional resources for Annual Review of Psychology, vol 51 2000
Into the cerebrospinal fluid space surrounding the lumbosacral cord (that is, to the spinal levels receiving sensation from the lower body), remarkable thermal hyperalgesia results (Watkins & Maier 1999b; ED Milligan, K Mehmert, JL Hinde, D Martin, SF Maier, et al, submitted for publication). Altered responsivity extends beyond thermal stimuli. t. administration, gp120 induces allodynia as well (Milligan et al 1998, 1999; Watkins & Maier 1999b). Thus, gp120, like peripheral immune activation by infection and injury, alters responsivity in ways paralleling clinically relevant aspects of pain.
That is, that proinflammatory cytokines again play a pivotal role. Within the brain, glia (which are immune-like cells of the central nervous system) respond to immune-to-brain signaling by synthesizing IL-1 de novo (Laye et al 1995). 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.
As noted previously, this pattern of effects predicts glial activation at spinal levels. In none of these cases has the effect Annu. Rev. Psychol. 51:29-57. org by Ball State University on 01/08/09. 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).