Abstract
To evaluate the role of serotonin and the vagal afferent nerves on preinflammatory responses (such as fever and feed-suppression) induced by inflammation broken out within the peritoneal cavity, we observed core temperature (TC) and food-intake (FI) in the Wistar strain rat after an administration of lipopolysaccaride (LPS) with or without ramosetron (a serotonin-3 type receptor antagonist). An administration of 100 μg/kg LPS elevated TC and suppressed FI with increase in afferent vagal nerve activity. Such LPS-induced fever and feed-suppression were completely abolished by the combined vagotomy in hepatic and bilateral gastric branches. Furthermore, the LPS-induced preinflammatory responses were prevented significantly by a pretreatment with 30 μg/kg ramosetron given into the peritoneal cavity before the pyrogenic challenge. These data suggest 1) that vagal afferent nerves convey an inflammatory signal to the central nervous system via the vagal hepatic and gastric branch and 2) that LPS was recognized by immune sensitive cells (e.g., dendritic cells) or testing cells (e.g., basal-granulated cells) when LPS-evoked preinflammation broke out in the peritoneal region and 3) that 5HT may transmit the LPS-evoked preflammatory signal via the 5HT-3 type receptors located in vagal afferent nerve terminals. [J Physiol Sci. 2008;58 Suppl:S155]
