Flood J F, Morley J E
Geriatric Research, Education and Clinical Center, Veterans Administration Hospital, Sepulveda, CA 91343.
Peptides. 1989 Jul-Aug;10(4):809-13. doi: 10.1016/0196-9781(89)90118-6.
Ingestion of food in mice following training on T-maze footshock avoidance enhanced memory retention when tested 7 days later. This eating-induced improvement of retention was blocked by a specific cholecystokinin antagonist, L-364,718. The cholecystokinin antagonist prevented enhancement of memory retention resulting from posttraining administration of the gastrointestinal hormones, cholecystokinin, bombesin or gastrin releasing peptide. L-364,718 neither impaired or improved retention when given alone. Specificity of the effect of L-364,718 was demonstrated by the failure of L-364,718 to block improved memory retention resulting from administration of arecoline and D-amphetamine. The studies provide evidence that activation of cholecystokinin receptors plays a physiological role in the mediation of meal-induced enhancement of memory retention.
在T型迷宫足部电击回避训练后摄入食物的小鼠,在7天后进行测试时,其记忆保持能力得到增强。这种由进食引起的记忆保持改善被一种特异性胆囊收缩素拮抗剂L-364,718所阻断。胆囊收缩素拮抗剂可阻止因训练后给予胃肠激素胆囊收缩素、蛙皮素或胃泌素释放肽而导致的记忆保持增强。单独给予L-364,718时,既不会损害也不会改善记忆保持。L-364,718未能阻断因给予槟榔碱和右旋苯丙胺而导致的记忆保持改善,从而证明了其作用的特异性。这些研究提供了证据,表明胆囊收缩素受体的激活在进食诱导的记忆保持增强的介导中发挥生理作用。