INTERLEUKIN-1 INCREASES ACTIVITY OF THE GASTRIC VAGAL AFFERENT NERVE PARTLY VIA STIMULATION OF TYPE-A CCK RECEPTOR IN ANESTHETIZED RATS

The response of mass activity of the gastric vagal afferent nerve to i ntravenous administration of interleukin-1 beta (IL-1 beta) and the in volvement of cholecystokinin (CCK) in the response were investigated i n pentobarbital-anesthetized rats. Intravenous administration of 2 mu g . kg(-1) of IL-1 beta caused an increase in the afferent activity, w hich reached 150% of control activity by 30 min after administration a nd persisted for more than 80 min. The increase in the nerve activity was significantly reduced in animals pretreated with a type A CCK rece ptor antagonist. IL-1 beta also significantly increased the CCK concen tration in systemic blood. Furthermore, it was confirmed that intraven ous administration of CCK produced an increase in the nerve activity v ia the type A CCK receptor. These findings suggest that systemically a pplied IL-1 beta increases CCK concentration in systemic blood secrete d from mucosal endocrine cells of the small intestine, and that in tur n CCK in the gastric blood flow augments or partly participates in the IL-1 beta-induced excitation of the gastric vagal afferent nerve via stimulation of the type A CCK receptor in the stomach. A possible invo lvement of IL-1-related excitation of the gastric vagal afferent nerve in IL-1-induced anorexia is discussed.