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http://purl.uniprot.org/citations/17506933http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Aim

To elucidate the role of scaffold protein postsynaptic density (PSD)-95 in the dopamine D1 receptor (D1R)-modulated NR1a/NR2B receptor response.

Methods

The human embryonic kidney 293 cells expressing D1R (tagged with the enhanced yellow fluorescent protein) and NR1a/NR2B with or without co-expression of PSD-95 were used in the experiments. The Ca2+ influx measured by imaging technique was employed to monitor N-methyl-D-aspartic acid receptors (NMDAR) function.

Results

The application of dopamine (DA, 100 micromol/L) did not alter glutamate/glycine (Glu/Gly)-induced NMDAR-mediated Ca2+ influx in cells only expressing the D1R/NR1a/NR2B receptor. However, DA increased Glu/Gly-induced Ca2+ influx in a concentration-dependent manner while the cells were co-expressed with PSD-95. D1R-stimulated Ca2+ influx was inhibited by a selective D1R antagonist SCH23390. Moreover, pre-incubation with either the protein kinase A (PKA) inhibitor H89, or the protein kinase C (PKC) inhibitor chelerythrine attenuated D1R-enhanced Ca2+ influx induced by the N-methyl-D-aspartic acid (NMDA) agonist. The results clearly indicate that D1R-modulated NR1a/NR2B receptor function depends on PSD-95 and is subjected to the regulation of PKA and PKC.

Conclusion

The present study provides the first evidence that PSD-95 is essential in D1R-regulated NR1a/NR2B receptor function."xsd:string
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http://purl.uniprot.org/citations/17506933http://purl.uniprot.org/core/author"Jin G.Z."xsd:string
http://purl.uniprot.org/citations/17506933http://purl.uniprot.org/core/author"Zhen X.C."xsd:string
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http://purl.uniprot.org/citations/17506933http://purl.uniprot.org/core/title"Requirement of PSD-95 for dopamine D1 receptor modulating glutamate NR1a/NR2B receptor function."xsd:string
http://purl.uniprot.org/citations/17506933http://purl.uniprot.org/core/volume"28"xsd:string
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