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D2 Dopamine Receptor-Deficient Mutant Mice

Tools to tease apart receptor subtype electrophysiology

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The Basal Ganglia VI

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 54))

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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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Levine, M.S., Cepeda, C., Hurst, R.S., Ariano, M.A., Low, M.J., Grandy, D.K. (2002). D2 Dopamine Receptor-Deficient Mutant Mice. In: Graybiel, A.M., Delong, M.R., Kitai, S.T. (eds) The Basal Ganglia VI. Advances in Behavioral Biology, vol 54. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0179-4_51

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