{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T02:11:04Z","timestamp":1787019064634,"version":"build-2736575974"},"reference-count":76,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2007,10,2]],"date-time":"2007-10-02T00:00:00Z","timestamp":1191283200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuroscientist"],"published-print":{"date-parts":[[2008,2]]},"abstract":"<jats:p>\n                    During disease, infection, or trauma, the cytokine tumor necrosis factor\n                    <jats:sub>\u03b1<\/jats:sub>\n                    (TNF\n                    <jats:sub>\u03b1<\/jats:sub>\n                    ) 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\n                    <jats:sub>\u03b1<\/jats:sub>\n                    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\n                    <jats:sub>\u03b1<\/jats:sub>\n                    . 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\n                    <jats:sub>\u03b1<\/jats:sub>\n                    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\n                    <jats:sub>\u03b1<\/jats:sub>\n                    receptors on these afferents and their ability to amplify afferent signals may explain how TNF\n                    <jats:sub>\u03b1<\/jats:sub>\n                    can completely disrupt autonomic control of the gut. NEUROSCIENTIST 14(1):53\u201467, 2008. 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