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Implications of Immune-to-Brain Communication for Sickness and Pain
Pages 7710-7713

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From page 7710...
... Fever is a phylogenetically very old response that raises the core body temperature to the point where bacteria/viruses do not multiple rapidly, bacteria cannot form protective outer coats, where white blood cells do multiple very rapidly, destructive enzymes key for survival function most effectively, and so on. Every degree of fever requires a 10-l5~o increase in energy, and most of the components of the sickness response can be viewed as supporting this energetic requirement by either creating energy (hormones released by sickness free energy from bodily stores)
From page 7711...
... The pathway by which abdominal sickness signals elicit hyperalgesia has been at least partially mapped in the central nervous system, by using a combination of discrete lesions and expression of cFos, an immediate-early gene product used as a neuronal activation marker (184. From this work, the neural circuitry underlying sickness hyperalgesia was found to involve a nucleus tractus solitaries nucleus rapine magnus spinal cord dorsolateral funiculus circuit.
From page 7712...
... Neurotransmitters released by the centrifugal pathway combined with neuroexcitatory substances released by astrocytes and microglia create exaggerated pain responses. Thus, for this form of hyperalgesia at least, glia assume a new, pivotal role in the generation of exaggerated pain.
From page 7713...
... Colloquium Paper: Watkins and Maier Maier, S


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