Greenwood-Van Meerveld B, Barron K W
Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City 73109, USA.
Eur J Pharmacol. 1998 Apr 10;346(2-3):197-202. doi: 10.1016/s0014-2999(98)00071-5.
Vagal motor outflow from the dorsal vagal complex is important in the regulation of intestinal motility. The aim of our study was to test the hypothesis that within the dorsal vagal complex, tonic GABA(A)-receptor mediated neurotransmission modulates intestinal motility. The GABA(A) receptor antagonist, bicuculline (methiodide), was microinjected into the dorsal vagal complex, and the effects on small intestinal and colonic motility were investigated. Rats were anesthetized and the mean arterial pressure and heart rate were monitored. Jejunal and colonic motility were measured manometrically, and motility indices were calculated manually. Bicuculline at concentrations of 0.25 or 0.5 mM in 30 nl was microinjected bilaterally into the dorsal vagal complex through stereotaxically placed micropipettes. The injection sites were confirmed histologically using the dye Alcian Blue. Bicuculline (0.5 mM) inhibited spontaneous jejunal motility by 76.3%, colonic motility by 51.7%, mean arterial pressure by 23.3% and heart rate by 27.6%. The lower concentration of bicuculline (0.25 mM) showed no inhibitory effects on intestinal motility but decreased mean arterial blood pressure by 24.1% and heart rate by 13.6%. Bilateral cervical vagotomy attenuated the bicuculline (0.5 mM)-induced inhibition of spontaneous jejunal motility, whereas the bicuculline effect on colonic motility was unaffected. The results of this study show that GABA(A) receptor-mediated neurotransmission in the dorsal vagal complex is involved in autonomic integration of motility of the small intestine and colon. Furthermore, our results indicate that the dorsal vagal complex regulation of jejunal motility involves vagal outflow, whereas vagal pathways do not participate in the bicuculline-induced inhibition of colonic motility.
来自迷走神经背核复合体的迷走运动传出神经在肠道运动调节中起重要作用。我们研究的目的是验证以下假说:在迷走神经背核复合体内,持续性γ-氨基丁酸A(GABA(A))受体介导的神经传递调节肠道运动。将GABA(A)受体拮抗剂荷包牡丹碱(甲碘化物)微量注射到迷走神经背核复合体中,并研究其对小肠和结肠运动的影响。对大鼠进行麻醉并监测平均动脉压和心率。通过压力测定法测量空肠和结肠的运动,并手动计算运动指数。将浓度为0.25或0.5 mM的30 nl荷包牡丹碱通过立体定位放置的微量移液器双侧微量注射到迷走神经背核复合体中。使用阿尔新蓝染料通过组织学方法确认注射部位。荷包牡丹碱(0.5 mM)可使空肠自发运动抑制76.3%,结肠运动抑制51.7%,平均动脉压降低23.3%,心率降低27.6%。较低浓度的荷包牡丹碱(0.25 mM)对肠道运动无抑制作用,但可使平均动脉血压降低24.1%,心率降低13.6%。双侧颈迷走神经切断术减弱了荷包牡丹碱(0.5 mM)诱导的空肠自发运动抑制,而荷包牡丹碱对结肠运动的影响未受影响。本研究结果表明,迷走神经背核复合体内GABA(A)受体介导的神经传递参与小肠和结肠运动的自主整合。此外,我们的结果表明,迷走神经背核复合体对空肠运动的调节涉及迷走神经传出,而迷走神经通路不参与荷包牡丹碱诱导的结肠运动抑制。