Abstract

The generation of transgenic mice lacking specific dopamine (DA) receptor subtypes has allowed elucidation of receptor function in isolation. We have used DA receptor-deficient mice to test the hypothesis that D1 and D2 receptor families modulate glutamate receptor-mediated activity in opposite ways. Accordingly, D1 receptors enhance and D2 receptors reduce glutamatergic activity. Consistent with this hypothesis we found that D1 receptor-deficient mice have a reduced ability to enhance glutamate responses. In contrast D2 receptor-deficient mice display enhanced glutamatergic activity. This enhancement may be due to the lack of D2 receptors on corticostriatal terminals.

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