Dum J, Gramsch C, Herz A
Pharmacol Biochem Behav. 1983 Mar;18(3):443-7. doi: 10.1016/0091-3057(83)90467-7.
Experiments were performed to find biochemical evidence of an activation of endogenous opiate peptides in the brain by incentive reward. A method used to estimate specific in vivo opiate binding in rats using the labelled opiate agonist, 3H-etorphine, indicated a considerable reduction in opiate binding exclusively in the hypothalamus of non-deprived animals given a highly palatable food to eat for 20 min. Radioimmunoassay of the hypothalamus of rats under similar conditions found a pronounced drop in the concentration of beta-endorphin, but not in dynorphin, in the hypothalamus, indicating a release and breakdown of beta-endorphin. Therefore, the reduction in opiate binding in the hypothalamus may at least be partially explained by an occupation of opiate receptors by beta-endorphin, causing a reduced availability of receptors to etorphine. A possible role of hypothalamic beta-endorphin in the facilitation of reward pathways in the brain is discussed.
进行了实验以寻找激励性奖励激活大脑中内源性阿片肽的生化证据。一种使用标记的阿片激动剂3H-埃托啡来估计大鼠体内特定阿片结合的方法表明，给予非剥夺动物美味食物进食20分钟后，仅下丘脑的阿片结合显著减少。在类似条件下对大鼠下丘脑进行放射免疫分析发现，下丘脑β-内啡肽浓度明显下降，但强啡肽浓度未下降，这表明β-内啡肽的释放和分解。因此，下丘脑阿片结合的减少至少部分可以解释为β-内啡肽占据了阿片受体，导致埃托啡的受体可用性降低。本文讨论了下丘脑β-内啡肽在促进大脑奖励通路中的可能作用。
