LaBuda C J, Fuchs P N
Department of Psychology, University of Texas at Arlington, Arlington, TX 76019, USA.
Brain Res Bull. 2001 Aug;55(6):755-60. doi: 10.1016/s0361-9230(01)00569-x.
Previous researchers demonstrate an opioidergic involvement in the anxiolytic and rewarding actions of ethanol and diazepam. Therefore, to further characterize the role of the opioid system in the anxiolytic action of ethanol and diazepam, normal (C57BL/6J), hybrid (B6129F1) and mu-opioid receptor knockout mice were given i.p. ethanol (0, 1.0 or 1.6 g/kg) or diazepam (1.5 mg/kg). The anxiolytic properties of these agents were then tested in the elevated plus-maze. Additional ethanol-treated mu-opioid receptor knockout mice (1 g/kg) were pretreated with the kappa-opioid receptor antagonist nor-BNI (0 or 3 mg/kg) to assess the involvement of kappa-opioid activity in ethanol's anxiolytic actions. The anxiolytic action of ethanol and diazepam in the mu-opioid receptor knockout mouse did not differ from the effects obtained in normal mice and pretreatment with nor-BNI did not significantly attenuate ethanol's actions in mu-opioid receptor knockout mice. Thus, the anxiolytic actions of ethanol and diazepam appear to be independent of opioid system activity in the mu-opioid receptor knockout mouse.
先前的研究人员证明阿片肽能参与乙醇和地西泮的抗焦虑及奖赏作用。因此，为了进一步明确阿片系统在乙醇和地西泮抗焦虑作用中的角色，给正常（C57BL/6J）、杂种（B6129F1）和μ-阿片受体基因敲除小鼠腹腔注射乙醇（0、1.0或1.6 g/kg）或地西泮（1.5 mg/kg）。然后在高架十字迷宫中测试这些药物的抗焦虑特性。另外，给经乙醇处理的μ-阿片受体基因敲除小鼠（1 g/kg）预先注射κ-阿片受体拮抗剂nor-BNI（0或3 mg/kg），以评估κ-阿片活性在乙醇抗焦虑作用中的参与情况。乙醇和地西泮在μ-阿片受体基因敲除小鼠中的抗焦虑作用与在正常小鼠中获得的效果没有差异，并且用nor-BNI预处理并未显著减弱乙醇在μ-阿片受体基因敲除小鼠中的作用。因此，在μ-阿片受体基因敲除小鼠中，乙醇和地西泮的抗焦虑作用似乎独立于阿片系统活性。
