Possible involvement of the CCK receptor in the benzodiazepine antagonism to CCK in the mouse brain.

Possible involvement of the CCK receptor in the benzodiazepine antagonism to CCK in the mouse brain.
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CCK 受体可能参与了小鼠大脑中苯二氮卓类药物对 CCK 的拮抗作用。

DOI:
10.1254/jjp.43.67
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发表时间:
1987
期刊:
Japanese journal of pharmacology
影响因子:
--
通讯作者:
K. Kubota
K. Kubota
中科院分区:
--
文献类型:
--
作者:
K. Sugaya;I. Matsuda;K. Kubota

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腹腔注射外周组织胆囊收缩素(CCK)受体拮抗剂利血平和丙谷胺,剂量依赖性地抑制由脑池内注射CCK八肽(CCK 8)引起的饱腹感。腹腔注射地西泮(1 mg/kg)和/或苯二氮卓类拮抗剂Ro 15-1788(5 mg/kg)均能阻止1 μ g CCK 8引起的痛阈升高。然而,Ro 15-1788并不拮抗地西泮逆转CCK诱导的抗伤害作用的作用。Ro 15-1788还抑制CCK 8诱导的饱腹感。根据这些结果,认为本研究中观察到的苯二氮卓类和丙谷胺对CCK 8的拮抗作用似乎发生在CCK受体,而不是脑中的苯二氮卓类受体。
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.
丙谷胺拮抗胆囊收缩素对兔胆囊的刺激。
DOI: --
发表时间: 1984
影响因子: --
作者:
Kaplita,PV;Roebuck,BD
通讯作者: Roebuck,BD