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Striatal A2A adenosine receptor antagonism differentially modifies striatal glutamate outflow in vivo in young and
1Department of Preclinical and Clinical Pharmacology, University of Florence, Italy.
Abstract:
The effect of the adenosine A2A receptor antagonist SCH 58261 on glutamate release was investigated in the striatum of young and old rats by microdialysis experiments. SCH 58261 (50 nM) significantly decreased the spontaneous and K+-evoked glutamate outflow in young rats. In aged rats, spontaneous glutamate outflow was significantly reduced in comparison to young rats and SCH 58261 significantly increased spontaneous and K+-evoked glutamate outflow. It is suggested that the opposite effects of the A2A antagonist on glutamate outflow in young and aged rats can be respectively attributed to blockade of striatal A2A adenosine receptors located on glutamatergic terminals and on the striatal indirect output pathway.
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