Crawley J N, Schwaber J S
Peptides. 1983 Sep-Oct;4(5):743-7. doi: 10.1016/0196-9781(83)90030-x.
Cholecystokinin (CCK) has been implicated as a signal for the syndrome of satiety in a variety of species. Several lines of evidence point to a peripheral site of action for the behavioral effects of CCK. Peripheral CCK receptors appear to activate a gut-brain pathway involving the sensory fibers of the vagus nerve. To investigate the central anatomical substrate of this visceral-behavioral control system, the terminal regions of the sensory tract of the vagus were lesioned. Radiofrequency lesions of the nucleus tractus solitarius abolished the effects of acute doses of CCK on exploratory behaviors. Sham lesions had no effect on baseline exploratory behaviors and did not influence the ability of CCK to decrease spontaneous exploratory behaviors. These findings delineate the first central site along the ascending sensory pathway which appears to mediate the satiety-related behavioral effects of CCK.
胆囊收缩素（CCK）在多种物种中被认为是饱腹感综合征的信号。有几条证据指向CCK行为效应的外周作用位点。外周CCK受体似乎激活了一条涉及迷走神经感觉纤维的肠-脑通路。为了研究这个内脏-行为控制系统的中枢解剖学基础，对迷走神经感觉束的终末区域进行了损伤。孤束核的射频损伤消除了急性剂量CCK对探索行为的影响。假损伤对基线探索行为没有影响，也不影响CCK降低自发探索行为的能力。这些发现描绘了沿着上行感觉通路的第一个中枢位点，该位点似乎介导了CCK与饱腹感相关的行为效应。
