Wu P H, Coffin V L
Brain Res. 1984 Feb 27;294(1):186-9. doi: 10.1016/0006-8993(84)91329-5.
Brain [3H]diazepam and L-[3H]phenylisopropyladenosine binding sites in caffeine-treated (75 mg/kg/day, i.p. 12 days) and caffeine-withdrawn (30 days) rats were examined. Treatment with caffeine (75 mg/kg/day) for 12 days increases the Bmax (maximum binding capacity) for [3H]diazepam binding by 30.9% whereas the same treatment increased the Bmax for L-[3H]PIA binding by 120%. The Bmax for [3H]diazepam binding sites returns to slightly below control levels but L-[3H]PIA binding sites still remain elevated after 30 days of caffeine withdrawal. The up-regulation of [3H]diazepam binding sites seen in caffeine-treated rats may indicate an interaction between caffeine and benzodiazepines at the receptor level and it may account for the supersensitivity to benzodiazepines seen in behavioral testing.
对经咖啡因处理（75毫克/千克/天，腹腔注射，共12天）及咖啡因撤药（30天）的大鼠的脑内[3H]地西泮和L-[3H]苯异丙基腺苷结合位点进行了检测。以75毫克/千克/天的咖啡因处理12天，可使[3H]地西泮结合的Bmax（最大结合容量）增加30.9%，而相同处理可使L-[3H]PIA结合的Bmax增加120%。在咖啡因撤药30天后，[3H]地西泮结合位点的Bmax恢复至略低于对照水平，但L-[3H]PIA结合位点仍保持升高。在经咖啡因处理的大鼠中观察到的[3H]地西泮结合位点上调，可能表明咖啡因与苯二氮䓬类药物在受体水平存在相互作用，这可能解释了行为测试中观察到的对苯二氮䓬类药物的超敏反应。
