Bucinskaite V, Kurosawa M, Lundeberg T
Department of Physiology and Pharmacology, Karolinska Institutet, von Eulers väg 4, 171 77 Stockholm, Sweden.
Br J Pharmacol. 2000 Apr;129(8):1649-54. doi: 10.1038/sj.bjp.0703270.
It has been proposed that the vagus nerve plays a role in mediating cholecystokinin-8 (CCK-8) effect on such gastric functions as motility, emptying and gastric acid secretion. To examine the contribution of the efferent pathways in realizing these effects, efferent mass activity in the ventral gastric vagal nerve in Sprague-Dawley rats was recorded. Intravenous infusion of CCK-8 (0.1-1 nmol) suppressed the efferent activity. The effect of CCK-8 was significantly reduced in animals with total subdiaphragmatic vagotomy in comparison to those with partial vagotomy. Intravenous infusion of CCK(A) receptor antagonist L-364,718 (1-100x10(-6) g) blocked the response of vagal efferent activity to 0.1 nmol CCK-8, but the CCK(B) receptor antagonist L-365,260 (1-100x10(-6) g) did not in the conditions of either partial or total vagotomy. Intracisternal infusion of L-364,718 (1x10(-6) g) blocked the response of vagal efferent activity to 0.1 nmol CCK-8 i.v. Infusion of exogenous CCK-8 did not affect the activity of supradiaphragmatic vagal afferents. The results suggest that the effect of systemically administered CCK-8 on vagal efferent activity is mediated by both peripherally (subdiaphragmatically) and centrally localized CCK(A) receptors.
有人提出，迷走神经在介导胆囊收缩素-8（CCK-8）对诸如胃动力、排空及胃酸分泌等胃功能的影响中发挥作用。为了研究传出通路在实现这些效应中的作用，记录了Sprague-Dawley大鼠腹侧胃迷走神经的传出神经总体活动。静脉输注CCK-8（0.1 - 1 nmol）可抑制传出活动。与部分迷走神经切断的动物相比，完全膈下迷走神经切断的动物中CCK-8的效应显著降低。静脉输注CCK(A)受体拮抗剂L-364,718（1 - 100×10(-6) g）可阻断迷走神经传出活动对0.1 nmol CCK-8的反应，但在部分或完全迷走神经切断的情况下，CCK(B)受体拮抗剂L-365,260（1 - 100×10(-6) g）则不能阻断。脑池内输注L-364,718（1×10(-6) g）可阻断迷走神经传出活动对静脉注射0.1 nmol CCK-8的反应。输注外源性CCK-8不影响膈上迷走神经传入纤维的活动。结果表明，全身给药的CCK-8对迷走神经传出活动的影响是由外周（膈下）和中枢定位的CCK(A)受体介导的。
