| First Author | Butcher AJ | Year | 2009 |
| Journal | J Biol Chem | Volume | 284 |
| Issue | 25 | Pages | 17147-56 |
| PubMed ID | 19332541 | Mgi Jnum | J:151014 |
| Mgi Id | MGI:4352609 | Doi | 10.1074/jbc.M901031200 |
| Citation | Butcher AJ, et al. (2009) N-Methyl-D-aspartate Receptors Mediate the Phosphorylation and Desensitization of Muscarinic Receptors in Cerebellar Granule Neurons. J Biol Chem 284(25):17147-56 |
| abstractText | Changes in synaptic strength mediated by ionotropic glutamate N-methyl-d-asparate (NMDA) receptors is generally considered to be the molecular mechanism underlying memory and learning. NMDA receptors themselves are subject to regulation through signaling pathways that are activated by G-protein-coupled receptors (GPCRs). In this study we investigate the ability of NMDA receptors to regulate the signaling of GPCRs by focusing on the G(q/11)-coupled M(3)-muscarinic receptor expressed endogenously in mouse cerebellar granule neurons. We show that NMDA receptor activation results in the phosphorylation and desensitization of M(3)-muscarinic receptors through a mechanism dependent on NMDA-mediated calcium influx and the activity of calcium-calmodulin-dependent protein kinase II. Our study reveals a complex pattern of regulation where GPCRs (M(3)-muscarinic) and NMDA receptors can feedback on each other in a process that is likely to influence the threshold value of signaling networks involved in synaptic plasticity. |
