| First Author | Gainetdinov RR | Year | 2003 |
| Journal | Neuron | Volume | 38 |
| Issue | 2 | Pages | 291-303 |
| PubMed ID | 12718862 | Mgi Jnum | J:83191 |
| Mgi Id | MGI:2658700 | Doi | 10.1016/s0896-6273(03)00192-2 |
| Citation | Gainetdinov RR, et al. (2003) Dopaminergic supersensitivity in G protein-coupled receptor kinase 6-deficient mice. Neuron 38(2):291-303 |
| abstractText | Brain dopaminergic transmission is a critical component in numerous vital functions, and its dysfunction is involved in several disorders, including addiction and Parkinson's disease. Responses to dopamine are mediated via G protein-coupled dopamine receptors (D1-D5). Desensitization of G protein-coupled receptors is mediated via phosphorylation by members of the family of G protein-coupled receptor kinases (GRK1-GRK7). Here we show that GRK6-deficient mice are supersensitive to the locomotor-stimulating effect of psychostimulants, including cocaine and amphetamine. In addition, these mice demonstrate an enhanced coupling of striatal D2-like dopamine receptors to G proteins and augmented locomotor response to direct dopamine agonists both in intact and in dopamine-depleted animals. The present study indicates that postsynaptic D2-like dopamine receptors are physiological targets for GRK6 and suggests that this regulatory mechanism contributes to central dopaminergic supersensitivity. |
