Crawley J N
Peptides. 1985;6 Suppl 1:133-7. doi: 10.1016/0196-9781(85)90022-1.
The satiety syndrome induced by intraperitoneally administered cholecystokinin (CCK) requires an intact visceral sensory feedback system involving the afferent vagus nerve and the nucleus tractus solitarius (NTS). Since both the vagus and the NTS contain CCK, the vagal-NTS synapse could conceivably employ CCK as a transmitter. To test this hypothesis, CCK was injected directly into the NTS region in awake rats. CCK at doses of 1 ng, 10 ng, and 100 ng had no effect on food consumption or exploratory behaviors associated with the satiety syndrome. The acetylcholine agonist carbachol, injected directly into the NTS region, effectively mimicked the actions of intraperitoneally administered CCK on feeding and exploration. These data suggest that CCK is not the transmitter at the vagal-NTS site in the visceral sensory pathway projecting to brain regions mediating the reduced feeding and exploration actions of systemic CCK.
腹腔注射胆囊收缩素（CCK）所诱发的饱腹感综合征需要一个完整的内脏感觉反馈系统，该系统涉及传入迷走神经和孤束核（NTS）。由于迷走神经和孤束核中都含有CCK，因此可以想象迷走神经-孤束核突触可能使用CCK作为递质。为了验证这一假设，将CCK直接注射到清醒大鼠的孤束核区域。剂量为1 ng、10 ng和100 ng的CCK对与饱腹感综合征相关的食物消耗或探索行为没有影响。直接注射到孤束核区域的乙酰胆碱激动剂卡巴胆碱有效地模拟了腹腔注射CCK对进食和探索的作用。这些数据表明，在投射到介导全身CCK减少进食和探索作用的脑区的内脏感觉通路中，CCK不是迷走神经-孤束核部位的递质。
