Schwartz G J, Tougas G, Moran T H
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Peptides. 1995;16(4):707-11. doi: 10.1016/0196-9781(95)00033-g.
The neurophysiological responses to 0.1 ml duodenal balloon inflation, 0.5 ml duodenal loads of normal saline, and 100 pmol close celiac arterial infusions of cholecystokinin (CCK) were obtained from 14 left cervical vagal afferent fibers in 14 rats. Duodenal, but not gastric, loads increased discharge rates in these slowly adapting fibers. CCK alone excited these fibers, and CCK pretreatment amplified subsequent duodenal load responses. Furthermore, duodenal loads generated greater responses when combined with CCK infusions. The small (< 3 mm) receptive fields of these fibers were localized to the ventral wall of the proximal duodenum, with C fiber conduction velocities (< 2 m/s). These results demonstrate for the first time rat duodenal load-sensitive vagal afferents. They can integrate signals arising from CCK and duodenal loads, and may mediate aspects of the role of CCK in the inhibition of gastric emptying and the control of food intake.
从14只大鼠的14条左颈迷走传入纤维获取了对0.1毫升十二指肠球囊扩张、0.5毫升十二指肠生理盐水负荷以及100皮摩尔腹腔动脉近距离注射胆囊收缩素(CCK)的神经生理反应。十二指肠负荷而非胃负荷增加了这些慢适应性纤维的放电率。单独的CCK可兴奋这些纤维,且CCK预处理可增强随后的十二指肠负荷反应。此外,十二指肠负荷与CCK注射联合时产生的反应更大。这些纤维的小(<3毫米)感受野定位于十二指肠近端的腹侧壁,C纤维传导速度(<2米/秒)。这些结果首次证明了大鼠十二指肠负荷敏感的迷走传入神经。它们可整合来自CCK和十二指肠负荷的信号,并可能介导CCK在抑制胃排空和控制食物摄入中的作用。