Download Annual Review of Psychology, vol 51 2000 by Janet T. Spence PDF

By Janet T. Spence

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Extra resources for Annual Review of Psychology, vol 51 2000

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Org by Ball State University on 01/08/09. For personal use only. 46 WATKINS Ⅲ MAIER This leads to the hypothesis that exaggerated pain would be expected to occur on infection of the spinal cord. A number of bacteria and viruses are neurotropic; that is, they ‘‘home’’ to the central nervous system and invade it. An example of one such virus is HIV-1, the virus that causes AIDS in humans. Various strains of HIV1 infect the brain and spinal cord early in the course of the disease and continue throughout disease progression (Diederich et al 1988).

G. heat, crush, pinprick, acid), and this activation causes these nerves to relay electrical signals to neurons in the spinal cord dorsal horns. Here, the incoming sensory nerve fibers synapse, so neurotransmitters released in response to the incoming electrical signals carry the pain message forward to the second neuron in line. These spinal cord dorsal horn neurons become activated in turn, causing electrical signals encoding the pain message to be sent up to the brain, toward consciousness (Figure 1).

Activation of these brain circuits leads to the release of IL-1 from glia, leading to the production of sickness responses. cells) (Goehler et al 1999). These immune cells respond to localized immune challenge by rapidly producing and releasing proinflammatory cytokines and other substances (Goehler et al 1999). Taken together, this immune-to-vagus-to-brain pathway appears to form a rapid response system for triggering brain-mediated sickness responses (Figure 2). Given that sensory vagal fibers synapse predominantly in the nucleus tractus solitarius (see Figure 2) (Ritter et al 1992), it would not be surprising if this medullary structure played a key role in the generation of brain-mediated sickness responses.

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