Wilson M C, Denson D, Bedford J A, Hunsinger R N
Peptides. 1983 May-Jun;4(3):351-7. doi: 10.1016/0196-9781(83)90146-8.
The current study involves an investigation of the possible neurotransmitter systems involved in the ability of exogenously administered sincalide (cholecystokinin octapeptide, CCK-8) to suppress feeding. Male rats previously trained to obtain food either during a daily 3-hr session, or conditioned to obtain food pellets on a fixed-ratio or fixed-interval schedule of reinforcement, were treated IP with CCK-8, following pretreatment with representative drugs of several pharmacological classes. Pretreatment with phenoxybenzamine, tolazoline, yohimbine, morphine, haloperidol or picrotoxin reduced the efficacy of CCK-8. However, pretreatment with naloxone or clonidine potentiated the suppressant action of CCK-8 on feeding. Propranolol, diphenhydramine, cimetidine, atropine, d-amphetamine, fenfluramine or diazepam pretreatment either had no effect or no consistent action in altering the activity of CCK-8. The ability of CCK-8 to suppress feeding was not altered by subacute treatment with the anorectics, d-amphetamine or fenfluramine, using a regimen known to induce tolerance. These data indicate that CCK-8 exerts a different mechanism of action than that of fenfluramine or d-amphetamine, and furthermore, that noradrenergic, dopaminergic, GABAergic or endogenous opioid systems either mediate or can modify the effect of CCK-8 on feeding.
当前的研究涉及对参与外源性施用辛卡利特（胆囊收缩素八肽，CCK - 8）抑制进食能力的可能神经递质系统的调查。先前经过训练在每日3小时时段获取食物，或经条件训练按固定比率或固定间隔强化程序获取食丸的雄性大鼠，在用几种药理学类别的代表性药物进行预处理后，腹腔注射CCK - 8。用酚苄明、妥拉唑啉、育亨宾、吗啡、氟哌啶醇或印防己毒素预处理会降低CCK - 8的效力。然而，用纳洛酮或可乐定预处理会增强CCK - 8对进食的抑制作用。用普萘洛尔、苯海拉明、西咪替丁、阿托品、右旋苯丙胺、芬氟拉明或地西泮预处理在改变CCK - 8的活性方面要么没有作用，要么没有一致的作用。使用已知会诱导耐受性的方案，用厌食药右旋苯丙胺或芬氟拉明进行亚急性治疗不会改变CCK - 8抑制进食的能力。这些数据表明，CCK - 8发挥的作用机制与芬氟拉明或右旋苯丙胺不同，此外，去甲肾上腺素能、多巴胺能、γ - 氨基丁酸能或内源性阿片样物质系统要么介导要么可以改变CCK - 8对进食的影响。
