Goldstein J M, Sutton E B, Malick J B
Life Sci. 1986 Feb 3;38(5):459-63. doi: 10.1016/0024-3205(86)90071-8.
Ro 15-1788 (10 mg/kg, ip) and CGS 8216 (10 mg/kg, ip) significantly reversed the inhibitory effect of diazepam (5 mg/kg, ip) on electrically induced head-turning in rats. Neither antagonist alone, at the dose level which blocked diazepam, had any intrinsic activity in this model. The specificity of the interaction between CGS 8216 and diazepam was further confirmed by the lack of antagonism by CGS 8216 of muscimol's inhibitory effect on head-turning. These results provide additional evidence that the inhibition of head-turning induced by diazepam is mediated via the benzodiazepine binding site. Furthermore, this model provides a functional expression of the interaction between the benzodiazepine recognition site, the chloride ionophore, and the GABA receptor complex.
Ro 15 - 1788（10毫克/千克，腹腔注射）和CGS 8216（10毫克/千克，腹腔注射）能显著逆转地西泮（5毫克/千克，腹腔注射）对大鼠电诱导转头行为的抑制作用。在能阻断地西泮作用的剂量水平下，单独使用这两种拮抗剂在该模型中均无任何内在活性。CGS 8216对蝇蕈醇抑制转头行为的作用无拮抗作用，进一步证实了CGS 8216与地西泮之间相互作用的特异性。这些结果提供了额外的证据，表明地西泮诱导的转头抑制是通过苯二氮䓬结合位点介导的。此外，该模型提供了苯二氮䓬识别位点、氯离子载体和GABA受体复合物之间相互作用的功能性表达。
