Neuronal cholecystokinin-like immunoreactivity is postprandially released from primate hypothalamus.
Neuronal cholecystokinin-like immunoreactivity is postprandially released from primate hypothalamus.
复制标题
灵长类下丘脑餐后释放神经元胆囊收缩素样免疫反应性。
DOI：
10.1016/0006-8993(87)90957-7
复制
发表时间：
1987
期刊：
影响因子：
2.9
通讯作者：
Go,VL
中科院分区：
文献类型：
--
作者：
Schick,RR;Reilly,WM;Roddy,DR;Yaksh,TL;Go,VL
采用推挽灌流技术，观察了食入食物后猫头鹰猴下丘脑神经元胆囊收缩素样免疫反应性（CCK-LI）的释放。在禁食过夜、氟烷麻醉的猫头鹰猴中，下丘脑推拉灌流液中的CCK-LI水平低于测定灵敏度（<4pg/30 min）。灌胃碳水化合物/氨基酸餐后，在第一个餐后30 min内，15个灌流部位中有5个的CCK-LI释放量增加了10倍（51 ± 7 pg/30 min），在随后的两个30 min间隔内，CCK-LI的释放量仍然增加，分别为32 ± 5 pg/30 min和15 ± 6pg/30 min。此后，CCK-LI释放再次低于测定灵敏度。在灌流液中加入40 mM氯化钾（KCl），引起神经元去极化，导致CCK-LI释放的第二次增加为56 ± 7 pg/30 min，与膳食诱导的释放相当。CCK-LI增高的部位均位于下丘脑前外侧。在实验中没有膳食诱导的释放，KCl没有任何影响CCK-LI在灌流液中，这表明这些特定的网站不包含CCK释放终端。高效液相色谱法（HPLC）鉴定了CCK的C-末端八肽（CCK-8）是猫头鹰猴下丘脑中CCK的主要分子形式。不存在胃泌素-17。本研究将先前报道的猫的发现扩展到灵长类动物，即（1）下丘脑中释放CCK的神经元被胃进食负荷产生的刺激激活，（2）进一步支持下丘脑中神经元CCK可能发挥与进食终止相关的生理作用的假设。
By use of the push-pull perfusion technique, release of neuronal cholecystokinin-like immunoreactivity (CCK-LI) from hypothalamus of owl monkeys was investigated in relation to an intragastric meal. In overnight fasted, halothane-anesthetized owl monkeys, levels of CCK-LI in the hypothalamic push-pull perfusate were below assay sensitivity (<4pg/30min). After intragastric administration of a carbohydrate/amino acid meal, however, a 10-fold increase in CCK-LI release (51 ± 7pg/30min) was observed in 5 out of 15 perfusion sites during the first postprandial 30 min. During the subsequent two 30-min intervals, release of CCK-LI was still increased with 32 ± 5pg/30min and 15 ± 6pg/30min, respectively. Thereafter, CCK-LI release was below assay sensitivity again. Addition of 40 mM potassium chloride (KCl) to the perfusion solution, which causes neuronal depolarization, resulted in a second increase in CCK-LI release of 56 ± 7pg/30min which was comparable to the meal-induced release. All sites that exhibited an increase in CCK-LI were located in the anterolateral aspect of the hypothalamus. In experiments without meal-induced release, KCl did not have any effect on CCK-LI in perfusate, suggesting that these particular sites did not contain CCK-releasing terminals. High performance liquid chromatography (HPLC) identified the C-terminal octapeptide of CCK (CCK-8) as the predominant molecular form of CCK within the owl monkey hypothalamus. No gastrin-17 was present. This study extends previously reported findings in cats to a primate species that (1) neurons which release CCK in hypothalamus are activated by stimuli generated by a gastric meal load, and (2) further supports the hypothesis that neuronal CCK within the hypothalamus may play a physiological role which correlates with the termination of feeding.