β-Arrestin-Dependent Dopaminergic Regulation of Calcium Channel Activity in the Axon Initial Segment

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

27 Scopus Citations
View graph of relations

Author(s)

  • Roy Ben-Shalom
  • Misol Ahn
  • Alayna T. Liptak
  • Richard M. van Rijn
  • Jennifer L. Whistler
  • Kevin J. Bender

Related Research Unit(s)

Detail(s)

Original languageEnglish
Pages (from-to)1518-1526
Journal / PublicationCell Reports
Volume16
Issue number6
Online published21 Jul 2016
Publication statusPublished - 9 Aug 2016

Link(s)

Abstract

G-protein-coupled receptors (GPCRs) initiate a variety of signaling cascades, depending on effector coupling. β-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. β-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 β-arrestin-dependent signaling to regulate neuronal excitability remains unclear. Here, we find that D3 dopamine receptors (D3R) regulate axon initial segment (AIS) excitability through β-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.

Research Area(s)

Citation Format(s)

β-Arrestin-Dependent Dopaminergic Regulation of Calcium Channel Activity in the Axon Initial Segment. / Yang, Sungchil; Ben-Shalom, Roy; Ahn, Misol et al.
In: Cell Reports, Vol. 16, No. 6, 09.08.2016, p. 1518-1526.

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

Download Statistics

No data available