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.