Li B H, Rowland N E
Department of Psychology, University of Florida, Gainesville 32611-2065.
Regul Pept. 1994 Mar 17;50(3):223-33. doi: 10.1016/0167-0115(94)90003-5.
It has been proposed that there might be a link between the anorectic actions of cholecystokinin (CCK) and serotonin (5HT). The present study compared the patterns of c-fos protein-like immunoreactivity (FLI) induced in rat brain by CCK and the indirect 5HT agonist dexfenfluramine (DFEN), as well as the ability for devazepide, a CCK-A receptor antagonist, to antagonize both anorexia and FLI induced by these agents. Devazepide reversed the anorectic effect of CCK but not that of DFEN in food deprived rats. The FLI induced by CCK and DFEN occurred in similar brain regions, but in different subdivisions. Such regions included the bed nucleus of the stria terminalis (BST), the lateral central nucleus of the amygdala (CeL), and the lateral parabrachial nucleus (LPB). Devazepide abolished the FLI induced by CCK in most of these brain regions, but had no effect on FLI induced by DFEN. These results suggest that the LPB-CeL/BST pathway might be responsible for the anorectic effects of both CCK and DFEN, but different parts or neuronal populations in these structures might be differentially engaged by CCK and DFEN. The putative interaction between CCK and 5HT might happen along this pathway, rather than in the periphery.
有人提出胆囊收缩素（CCK）的厌食作用与血清素（5HT）之间可能存在联系。本研究比较了CCK和间接5HT激动剂右芬氟拉明（DFEN）在大鼠脑中诱导的c-fos蛋白样免疫反应（FLI）模式，以及CCK-A受体拮抗剂德伐西匹拮抗这些药物诱导的厌食和FLI的能力。在饥饿大鼠中，德伐西匹逆转了CCK的厌食作用，但没有逆转DFEN的厌食作用。CCK和DFEN诱导的FLI出现在相似的脑区，但在不同的亚区。这些区域包括终纹床核（BST）、杏仁核外侧中央核（CeL）和外侧臂旁核（LPB）。德伐西匹在这些脑区中的大多数区域消除了CCK诱导的FLI，但对DFEN诱导的FLI没有影响。这些结果表明，LPB-CeL/BST通路可能是CCK和DFEN厌食作用的原因，但这些结构中的不同部分或神经元群体可能被CCK和DFEN以不同方式激活。CCK和5HT之间的假定相互作用可能发生在这条通路上，而不是在外周。
