Sugaya K, Matsuda I, Kubota K
Jpn J Pharmacol. 1987 Jan;43(1):67-71. doi: 10.1254/jjp.43.67.
In mice, intraperitoneally injected chlordiazepoxide and proglumide, both of which are regarded as cholecystokinin (CCK) receptor antagonists in the peripheral tissues, dose-dependently inhibited the satiety induced by 200 ng of intracisternally administered CCK octapeptide (CCK8). Intraperitoneally administered diazepam (1 mg/kg) and/or Ro 15-1788 (5 mg/kg), a benzodiazepine antagonist, both prevented the elevation in the pain threshold induced by 1 microgram of CCK8. However, Ro 15-1788 did not antagonize the effect of diazepam that reversed the CCK-induced antinociception. Ro 15-1788 also inhibited the satiety induced by CCK8. From these results, it was considered that the antagonism, which was observed in the present work, of benzodiazepines and proglumide to CCK8 seemed to occur at the CCK receptor and not at the benzodiazepine receptor in the brain.
在小鼠中，腹腔注射氯氮卓和丙谷胺，这两种药物在周围组织中均被视为胆囊收缩素（CCK）受体拮抗剂，它们能剂量依赖性地抑制脑池内注射200纳克CCK八肽（CCK8）所诱导的饱腹感。腹腔注射地西泮（1毫克/千克）和/或苯二氮卓拮抗剂Ro 15 - 1788（5毫克/千克），均能防止1微克CCK8所诱导的痛阈升高。然而，Ro 15 - 1788并不拮抗地西泮逆转CCK诱导的抗伤害感受的作用。Ro 15 - 1788也抑制CCK8所诱导的饱腹感。从这些结果来看，本研究中观察到的苯二氮卓类药物和丙谷胺对CCK8的拮抗作用似乎发生在CCK受体而非脑中的苯二氮卓受体上。
