Qian M, Zhu S W, Johnson A E, Södersten P
Section of Applied Neuroendocrinology, Karolinska Institutet, Huddinge, Sweden.
Neuroreport. 2000 Aug 21;11(12):2617-20. doi: 10.1097/00001756-200008210-00002.
Satiety signals from the gastrointestinal tract travel via vagal afferents to the nucleus of the solitary tract (NTS) in the brain stem, the first central relay in a neural network which controls food intake. The non-competitive NMDA antagonist MK-801 facilitates food intake in rats by acting on the NTS. Here we report that hepatic portal vein infusion of MK-801 (25 or 50 microg/kg) increases intake of an intraorally infused 1 M solution of sucrose (by 113 +/- 9 and 132 +/- 11%, respectively) and that this effect is prevented by hepatic vagotomy. By contrast, jugular vein infusion of MK-801 fails to increase sucrose intake but induces forward locomotion, indicating activation of a central mechanism. These data suggest that MK-801 can stimulate food intake by acting peripherally on hepatic vagal afferents.
来自胃肠道的饱腹感信号通过迷走神经传入纤维传递到脑干的孤束核（NTS），孤束核是控制食物摄入的神经网络中的第一个中枢中继站。非竞争性NMDA拮抗剂MK-801通过作用于孤束核促进大鼠的食物摄入。在此我们报告，经肝门静脉输注MK-801（25或50微克/千克）可增加经口输注的1 M蔗糖溶液的摄入量（分别增加113±9%和132±11%），并且肝迷走神经切断术可阻止这种效应。相比之下，经颈静脉输注MK-801未能增加蔗糖摄入量，但会诱发向前运动，表明激活了一种中枢机制。这些数据表明，MK-801可通过外周作用于肝迷走神经传入纤维来刺激食物摄入。
