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目的 研究多巴胺受体激动剂对乙醇引起大鼠纹状体抗坏血酸 (AA)释放的影响。方法 应用脑内透析技术结合高效液相电化学检测的方法。结果 乙醇 (3 0 g·kg-1,ip)显著增加纹状体抗坏血酸释放 ,高于基础水平的 2 0 0 %左右。多巴胺D1受体激动剂SKF 38393(10mg·kg-1,ip)对纹状体AA释放及乙醇引起纹状体AA释放均无显著影响。多巴胺D2 受体激动剂LY 1715 5 5 (0 5 ,1 0mg·kg-1,ip)显著增加纹状体AA释放及乙醇引起纹状体AA释放 ,但LY1715 5 5与乙醇对纹状体抗坏血酸释放的增加没有协同作用。具有多巴胺D1受体强拮抗剂和D2 受体强激动剂特性的溴隐亭 (10mg·kg-1,ip)在给药后 6 0min内对纹状体AA释放及乙醇引起纹状体AA释放均有显著的增加作用 ,且两者有协同作用。非选择性多巴胺受体激动剂阿扑吗啡也能增加纹状体AA释放及乙醇引起纹状体AA释放 ,而 0 2mg·kg-1的阿扑吗啡与乙醇有协同作用 ,0 4,0 8mg·kg-1的阿扑吗啡与乙醇没有协同作用。结论 多巴胺D2 受体的兴奋参与调节纹状体AA的释放 ,兴奋D2 受体同时抑制D1受体能够协同乙醇引起的大鼠纹状体抗坏血酸释放的作用。
Objective To investigate the effects of dopamine receptor agonists on ethanol-induced release of striatal ascorbic acid (AA) in rats. Methods The method of intracerebral dialysis combined with high performance liquid electrochemistry was used. Results Ethanol (30 g · kg -1, ip) significantly increased striatal ascorbate release, which was about 200% higher than the baseline level. Dopamine D1 receptor agonist SKF 38393 (10 mg · kg-1, ip) had no significant effect on AA release in striatum and AA-induced striatal release by ethanol. Dopamine D2 receptor agonist LY 1715 5 5 (0 5, 10 mg · kg -1, ip) significantly increased the release of AA from the striatum and the AA-induced release of AA from the striatum, but LY1715 5 5 and ethanol inhibited striatal ascorbate The increase in release has no synergistic effect. Bromocriptine (10 mg · kg-1, ip), a potent dopamine D1 receptor antagonist and a D2 receptor agonist, exerted a striatal AA release within 60 min after administration and ethanol induced striatal AA release Have a significant increase in the role, and both have synergistic effects. Apomorphine, a nonselective dopamine receptor agonist, also increased AA release in striatum and AA in ethanol, whereas apomorphine at 0.2 mg · kg -1 had a synergistic effect with ethanol, 0 4,0 8 mg Apomorphine at a dose of kg-1 has no synergistic effect with ethanol. Conclusions The excitability of dopamine D2 receptor is involved in regulating the release of AA from the striatum. The excitement of D2 receptor and the suppressive effect of D1 receptor on the ethanol-induced striatal ascorbate release in rat striatum were also observed.