Abstract
The effect of the adenosine A2A receptor agonist CGS 21680 on glutamate and aspartate release was investigated in the striatum of young and old rats by microdialysis experiments. CGS 21680 (10 microM) significantly increased glutamate and aspartate spontaneous outflow in young but not in old rats. On the contrary, CGS 21680 induced the same decrease in K+-evoked glutamate outflow in both young and aged rats. A lower dose of CGS 21680 (1 microM) failed to modify either spontaneous or K+-evoked outflow. It is suggested that the opposite effects of the A2A agonist on excitatory amino acid outflow may be respectively mediated by striatal A2A adenosine receptors located on glutamatergic terminals and on the striatal indirect output pathway.
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