Kurosawa M, Uvnäs-Moberg K, Miyasaka K, Lundeberg T
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
J Auton Nerv Syst. 1997 Jan 12;62(1-2):72-8. doi: 10.1016/s0165-1838(96)00111-7.
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.
在戊巴比妥麻醉的大鼠中，研究了胃迷走神经传入神经的大量活动对静脉注射白细胞介素-1β（IL-1β）的反应以及胆囊收缩素（CCK）在该反应中的作用。静脉注射2微克·千克-1的IL-1β可引起传入活动增加，给药后30分钟时传入活动达到对照活动的150%，并持续超过80分钟。在用A型CCK受体拮抗剂预处理的动物中，神经活动的增加明显减少。IL-1β还显著增加了全身血液中的CCK浓度。此外，证实静脉注射CCK通过A型CCK受体使神经活动增加。这些发现表明，全身应用的IL-1β会增加小肠黏膜内分泌细胞分泌的全身血液中的CCK浓度，进而胃血流中的CCK通过刺激胃中的A型CCK受体增强或部分参与IL-1β诱导的胃迷走神经传入神经兴奋。讨论了IL-1相关的胃迷走神经传入神经兴奋在IL-1诱导的厌食症中的可能作用。
