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首页> 外文期刊>American Journal of Physiology >Characterization of mice lacking the gene for cholecystokinin
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Characterization of mice lacking the gene for cholecystokinin

机译：缺乏胆囊收缩素基因的小鼠的表征

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摘要

CCK is also a neurotransmitter in many areas of the nervous system (6). Intraperitoneal or central administration of either purified CCK extracts or synthetic CCK-8 to fasted rats reduces food intake (22, 33, 37, 54), and this is manifested by a reduction of meal size as opposed to reduced frequency of meals (22, 37). Two types of CCK receptors (CCK1 and CCK2) have been cloned (5, 7). Pretreatment of animals with a CCK1 receptor antagonist increases meal size, whereas a CCK2 receptor antagonist has no effect (5, 7). In addition, administration of exogenous CCK-8 does not reduce food intake in CCK1 receptor-deficient mice and rats, suggesting that the satiation effect of CCK-8 is mediated via CCK1 receptors (36, 49). The satiating effect of systemic CCK is attenuated by subdiaphragmatic vagotomy, by selective vagal deafferentation, or by deactivation of vagal afferents with capsaicin (5, 44, 48). The generally accepted model is that exogenous CCK-8 elicits a short-term satiation effect by stimulating CCK1 receptors on vagal afferent nerves projecting to the brain (5, 7, 22, 33, 37, 44, 48).
机译：CCK也是神经系统许多区域的神经递质（6）。向禁食大鼠腹腔或中央施用纯化的CCK提取物或合成CCK-8会减少食物摄入（22，33，37，54），这通过减少进餐量而不是减少进餐频率来体现（22， 37）。已克隆了两种类型的CCK受体（CCK1和CCK2）（5、7）。用CCK1受体拮抗剂预处理动物会增加进食量，而CCK2受体拮抗剂则没有作用（5、7）。另外，在缺乏CCK1受体的小鼠和大鼠中，外源CCK-8的给药不会减少食物摄入，这表明CCK-8的饱食作用是通过CCK1受体介导的（36，49）。通过dia肌下迷走神经切断术，迷走神经选择性脱除迷走神经或用辣椒素灭活迷走神经传入，减弱了全身性CCK的饱腹感（5，44，48）。普遍接受的模型是外源CCK-8通过刺激投射到大脑的迷走神经上的CCK1受体引起短期饱食作用（5、7、22、33、37、44、48）。

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