By Janet T. Spence
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Additional resources for Annual Review of Psychology, vol 51 2000
However, a variety of recent research suggests that the interaction between brain and body is far more dynamic than previously recognized, with peripheral systems and products exerting potent effects on neural processes and thereby behavior. This bidirectionality of communication has become clear with regard to interactions between the brain and the immune system. Initial interest in brain-immune relationships focused on how neural processes could regulate immune function, but it is now clear that immune products signal the central nervous system and regulate its activity (for review see Maier & Watkins 1998).
IL-1 exerts its effects on pain by selectively exaggerating neuronal electrical responses to intense stimuli applied to the skin (Oka et al 1994a). One site of IL-1 action is the hypothalamic preoptic area because microinjection of IL-1 into this site is sufficient to produce thermal hyperalgesia (Oka et al 1995a). v. 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).
CYTOKINES AND PAIN 35 Classically, hyperalgesia and allodynia have been assumed to be due entirely to alterations in neural function. For example, nerve crush or other trauma was thought to cause physical and functional changes in the membrane of the damaged nerve (Willis 1992). The abnormal nerve would then send barrages of electrical activity to spinal cord dorsal horn neurons, setting LTP-like processes within these neurons into motion. Thus, this view focused on direct damage to the nerve itself and the resulting neuronally mediated LTP-like cascades.
Annual Review of Psychology, vol 51 2000 by Janet T. Spence