Verbalis J G, McCann M J, McHale C M, Stricker E M
Science. 1986 Jun 13;232(4756):1417-9. doi: 10.1126/science.3715453.
Administration of cholecystokinin (CCK) to rats caused a dose-dependent increase in plasma levels of the neurohypophyseal hormone oxytocin (OT). The OT secretion was comparable to that found in response to nausea-producing chemical agents that cause learned taste aversions. The effect of CCK on OT secretion was blunted after gastric vagotomy, as was the inhibition of food intake induced by CCK. Food ingestion also led to elevated plasma OT in rats, but CCK and aversive agents caused even greater OT stimulation. Thus, after administration of large doses of CCK, vagally mediated activation of central nausea pathways seems to be predominantly responsible for the subsequent decrease in food intake. Despite their dissimilar affective states, both nausea and satiety may activate a common hypothalamic oxytocinergic pathway that controls the inhibition of ingestion.
给大鼠注射胆囊收缩素（CCK）会导致神经垂体激素催产素（OT）的血浆水平呈剂量依赖性升高。OT的分泌与对引起习得性味觉厌恶的致恶心化学物质的反应相当。胃迷走神经切断术后，CCK对OT分泌的作用减弱，CCK诱导的食物摄入抑制也减弱。食物摄入也会导致大鼠血浆OT升高，但CCK和厌恶剂会引起更大的OT刺激。因此，在大剂量注射CCK后，迷走神经介导的中枢恶心通路激活似乎是随后食物摄入量减少的主要原因。尽管恶心和饱腹感的情感状态不同，但它们都可能激活一条共同的下丘脑催产素能通路，该通路控制着对摄入的抑制。
