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This version was published on February 1, 2008
The Neuroscientist, Vol. 14, No. 1, 53-67 (2008)
DOI: 10.1177/1073858407305725

Reviews

TNF {alpha}: A Trigger of Autonomic Dysfunction

Gerlinda E. Hermann

Laboratory of Autonomic Neurosciences, Pennington Biomedical Research Center, Baton Rouge, Louisiana, HermanGE{at}pbrc.edu

Richard C. Rogers

Laboratory of Autonomic Neurosciences, Pennington Biomedical Research Center, Baton Rouge, Louisiana, RogersRC{at}pbrc.edu

During disease, infection, or trauma, the cytokine tumor necrosis factor{alpha} (TNF {alpha}) causes fever, fatigue, malaise, allodynia, anorexia, gastric stasis associated with nausea, and emesis via interactions with the central nervous system. Our studies have focused on how TNF{alpha} produces a profound gastric stasis by acting on vago-vagal reflex circuits in the brainstem. Sensory elements of this circuit (i.e., nucleus of the solitary tract [NST] and area postrema) are activated by TNF{alpha}. In response, the efferent elements (i.e., dorsal motor neurons of the vagus) cause gastroinhibition via their action on the gastric enteric plexus. We find that TNF{alpha} presynaptically modulates the release of glutamate from primary vagal afferents to the NST and can amplify vagal afferent responsiveness by sensitizing presynaptic intracellular calcium-release mechanisms. The constitutive presence of TNF{alpha} receptors on these afferents and their ability to amplify afferent signals may explain how TNF {alpha} can completely disrupt autonomic control of the gut. NEUROSCIENTIST 14(1):53—67, 2008. DOI: 10.1177/1073858407305725

Key Words: Immune-neural interactions • Gastric stasis • Visceral malaise • Hypersensitivity • Potentiation • Allodynia • Illness behavior


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