Abstract：
:Activation of immune cells by pathogens induces the release of a variety of proinflammatory cytokines, including IL-1 beta and TNF-alpha. Previous studies using IL-1 beta have demonstrated that this cytokine can alter brain function, resulting in a variety of 'illness responses' including increased sleep, decreased food intake, fever, etc. We have recently demonstrated that i.p. IL-1 beta also produces hyperalgesia and that this hyperalgesia (as well as most illness responses) is mediated via activation of subdiaphragmatic vagal afferents. The present series of studies were designed to provide an initial examination of the generality of proinflammatory cytokine-induced hyperalgesia by examining the effects of i.p. TNF-alpha on pain responsivity. These studies demonstrate that: (a) i.p. TNF-alpha produces dose-dependent hyperalgesia as measured by the tailflick test, (b) this hyperalgesia is mediated via the induced release of IL-1 beta, (c) hyperalgesia is mediated via activation of subdiaphragmatic vagal afferents, and (d) the effects of subdiaphragmatic vagotomy cannot be explained by a generalized depression of neural excitability.
journal_name
Brain Resjournal_title
Brain researchauthors
Watkins LR,Goehler LE,Relton J,Brewer MT,Maier SFdoi
10.1016/0006-8993(95)00715-3subject
Has Abstractpub_date
1995-09-18 00:00:00pages
244-50issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(95)00715-3journal_volume
692pub_type
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