ADENOSINE-A1 AND A2 RECEPTORS MODULATE EXTRACELLULAR DOPAMINE LEVELS IN RAT STRIATUM

To clarify differences in the operating mechanisms of adenosine recept or subtypes (Al and A2), striatal extracellular dopamine levels under various conditions were determined by in vivo microdialysis. Adenosine (50 mu M) as well as the selective Al agonist, 2-chloro-N-6-cyclopent yladenosine (CCPA; 1 mu M ) decreased striatal extracellular dopamine levels, while the selective adenosine Al antagonist, 8-cyclopentyl-1,3 -dimethylxanthine (CPT; 50 mu M) and caffeine (100 mu M) increased str iatal extracellular dopamine levels. A selective A2a agonist, hyl)phen ethylamino]-5'-N-ethylcarboxamideadenosine (CGS21680; 10 mu M), a sele ctive A2 agonist, 5-dimethoxyphenyl)-2-(methylphenyl)ethyl]adenosine ( DPMA; 5 mu M) and a selective A2 antagonist, 3,7-dimethyl-1-propargylx anthine (DMPX; 10 mu M), did not affect extracellular dopamine levels. When the Al receptor was blocked by CPT, extracellular dopamine level s were increased by adenosine and DPMA, decreased by caffeine as well as DMPX, and unaffected by CGS21680. These results indicate that the s timulatory effects of the A2 receptor on striatal extracellular dopami ne levels are masked by the inhibitory effects of the Al receptor.