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 intravenous administration of interleukin-1 beta (IL-1 beta) and the involvement of cholecystokinin (CCK) in the response were investigated in pentobarbital-anesthetized rats. Intravenous administration of 2 micrograms.kg-1 of IL-1 beta caused an increase in the afferent activity, which reached 150% of control activity by 30 min after administration and persisted for more than 80 min. The increase in the nerve activity was significantly reduced in animals pretreated with a type A CCK receptor antagonist. IL-1 beta also significantly increased the CCK concentration in systemic blood. Furthermore, it was confirmed that intravenous administration of CCK produced an increase in the nerve activity via the type A CCK receptor. These findings suggest that systemically applied IL-1 beta increases CCK concentration in systemic blood secreted from mucosal endocrine cells of the small intestine, and that in turn 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 involvement of IL-1-related excitation of the gastric vagal afferent nerve in IL-1-induced anorexia is discussed.

[1]  Y. Oomura,et al.  The effects of interleukin-1 beta on the activity of adrenal, splenic and renal sympathetic nerves in the rat. , 1991, Journal of the autonomic nervous system.

[2]  Y. Shimomura,et al.  Effects of Recombinant Human Interleukins on Food Intake of Previously Food-Deprived Rats , 1990, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[3]  M. Carlquist,et al.  Plasma concentrations of cholecystokinin, CCK-8, and CCK-33, 39 in rats, determined by a method based on enzyme digestion of gastrin before HPLC and RIA detection of CCK. , 1989, Gut.

[4]  D. Nance,et al.  Neural and biochemical mediators of endotoxin and stress-induced c-fos expression in the rat brain , 1994, Brain Research Bulletin.

[5]  P. McHugh,et al.  Pharmacological dissociation of responses to CCK and gastric loads in rat mechanosensitive vagal afferents. , 1994, The American journal of physiology.

[6]  A. Vander,et al.  Suppression of food intake during infection: is interleukin-1 involved? , 1985, The American journal of clinical nutrition.

[7]  C. Dinarello,et al.  Biology of interleukin 1 , 1988, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[8]  C. Plata-salamán,et al.  Tumor necrosis factor and interleukin-1β: suppression of food intake by direct action in the central nervous system , 1988, Brain Research.

[9]  G. T. Smith,et al.  Anatomic localization of cholecystokinin receptors to the pyloric sphincter. , 1984, The American journal of physiology.

[10]  G. P. Smith,et al.  Abdominal vagotomy blocks the satiety effect of cholecystokinin in the rat. , 1981, Science.

[11]  N. Sato,et al.  Effects of peripheral administration of recombinant human interleukin-1 beta on feeding behavior of the rat. , 1990, Life sciences.

[12]  L. Blackshaw,et al.  Effects of cholecystokinin (CCK-8) on two classes of gastroduodenal vagal afferent fibre. , 1990, Journal of the autonomic nervous system.

[13]  P. McHugh,et al.  Blockade of type A, not type B, CCK receptors attenuates satiety actions of exogenous and endogenous CCK. , 1992, The American journal of physiology.

[14]  P. McHugh,et al.  Transport of cholecystokinin (CCK) binding sites in subdiaphragmatic vagal branches , 1987, Brain Research.

[15]  D. McCarthy,et al.  The role of cholecystokinin in interleukin-1-induced anorexia , 1993, Physiology & Behavior.

[16]  S. Iversen,et al.  Evidence that decreased feeding induced by systemic injection of cholecystokinin is mediated by CCK-A receptors. , 1989, European journal of pharmacology.

[17]  L. Blackshaw,et al.  Locally and reflexly mediated effects of cholecystokinin-octapeptide on the ferret stomach. , 1991, Journal of the autonomic nervous system.

[18]  P. McHugh,et al.  Integration of vagal afferent responses to gastric loads and cholecystokinin in rats. , 1991, The American journal of physiology.

[19]  P. Sawchenko,et al.  A functional anatomical analysis of central pathways subserving the effects of interleukin-1 on stress-related neuroendocrine neurons , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[20]  A. Randich,et al.  Electrical stimulation of the subdiaphragmatic vagus in rats: inhibition of heat-evoked responses of spinal dorsal horn neurons and central substrates mediating inhibition of the nociceptive tail flick reflex , 1992, Pain.

[21]  G. Clarke,et al.  Mechanical properties and sensitivity to CCK of vagal gastric slowly adapting mechanoreceptors. , 1988, The American journal of physiology.

[22]  G. P. Smith,et al.  Afferent axons in abdominal vagus mediate satiety effect of cholecystokinin in rats. , 1985, The American journal of physiology.