| First Author | Yang S | Year | 2016 |
| Journal | Cell Rep | Volume | 16 |
| Issue | 6 | Pages | 1518-1526 |
| PubMed ID | 27452469 | Mgi Jnum | J:236928 |
| Mgi Id | MGI:5810231 | Doi | 10.1016/j.celrep.2016.06.098 |
| Citation | Yang S, et al. (2016) beta-Arrestin-Dependent Dopaminergic Regulation of Calcium Channel Activity in the Axon Initial Segment. Cell Rep 16(6):1518-26 |
| abstractText | G-protein-coupled receptors (GPCRs) initiate a variety of signaling cascades, depending on effector coupling. beta-arrestins, which were initially characterized by their ability to "arrest" GPCR signaling by uncoupling receptor and G protein, have recently emerged as important signaling effectors for GPCRs. beta-arrestins engage signaling pathways that are distinct from those mediated by G protein. As such, arrestin-dependent signaling can play a unique role in regulating cell function, but whether neuromodulatory GPCRs utilize beta-arrestin-dependent signaling to regulate neuronal excitability remains unclear. Here, we find that D3 dopamine receptors (D3R) regulate axon initial segment (AIS) excitability through beta-arrestin-dependent signaling, modifying CaV3 voltage dependence to suppress high-frequency action potential generation. This non-canonical D3R signaling thereby gates AIS excitability via pathways distinct from classical GPCR signaling pathways. |
