摘要
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。
AIM To study the effects of dopamine receptor agonists on ethanol induced striatal ascorbic acid(AA) release in rats. METHODS The microdialysis coupled to high performance liquid chromatography with electrochemical detection. RESULTS Ethanol(3 0 g·kg -1 , ip) stimulated significantly striatal AA release by morethan 200% above the baseline. SKF 38393(10 mg·kg -1 , ip), a D 1 dopamine receptor agonist, showed no effect on either basal or ethanol induced AA release. LY 171555 (0 5, 1 0 mg·kg -1 , ip), a D 2 dopamine receptor agonist, increased basal and ethanol induced striatal AA release, but both drugs had no synergistical interaction. Bromocription(10 mg·kg -1 , ip), a D 1 dopamine receptor antagonist and D 2 dopamine receptor agonist, increased the basal striatal AA release, and potentiated ethanol induced AA release synergistically during 60 min after ethanol injected. Apomorphine(0 2, 0 4, 0 8 mg·kg -1 , sc), nonselective dopamine receptor agonist , could also increase basal and ethanol induced AA release, and the lower dose(0 2 mg·kg -1 ) showed synergistical action. CONCLUSION The excitation of D 2 dopamine receptor should be involved in the regulation striatal AA release, and have synergistical interaction on ethanol induced AA release.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2000年第2期158-161,共4页
Chinese Pharmacological Bulletin
关键词
多巴胺受体激动剂
抗坏血酸
乙醇
纹状体
bromocription
apomorphine
LY 171555
SKF 38393
ascorbic acid
ethanol
striatum
microdialysis
