OXYTOCIN SECRETION IN RESPONSE TO CHOLECYSTOKININ AND FOOD - DIFFERENTIATION OF NAUSEA FROM SATIETY
OXYTOCIN SECRETION IN RESPONSE TO CHOLECYSTOKININ AND FOOD - DIFFERENTIATION OF NAUSEA FROM SATIETY
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DOI：
10.1126/science.3715453
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发表时间：
1986-06-13
期刊：
影响因子：
56.9
通讯作者：
STRICKER, EM
中科院分区：
文献类型：
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作者：
VERBALIS, JG;MCCANN, MJ;STRICKER, EM
大鼠给予CCK后，血浆中神经垂体激素催产素(OT)水平呈剂量依赖性升高。OT的分泌与对产生恶心的化学物质的反应相当，这些化学物质会导致后天的味道厌恶。胃迷走神经切断后，CCK对OT分泌的影响减弱，CCK对摄食的抑制作用也减弱。食物摄入也导致大鼠血浆OT升高，但CCK和厌恶药物引起更大的OT刺激。因此，在给予大剂量CCK后，迷走神经介导的中枢恶心通路的激活似乎是随后食物摄入量减少的主要原因。尽管它们的情感状态不同，但恶心和饱腹感都可能激活共同的下丘脑催产素能通路，控制对摄取的抑制。
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.