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Molecular basis for N-type voltage-gated Ca2+ channel modulation by Gq protein-coupled receptors

Title
Molecular basis for N-type voltage-gated Ca2+ channel modulation by Gq protein-coupled receptors
Authors
Keum, Dong IlSuh, Byung Chang
DGIST Authors
Keum, Dong Il; Suh, Byung Chang
Issue Date
2015
Citation
Receptors & Clinical Investigation, 2(1), e515-e515
Type
Article
ISSN
2330-0566
Abstract
N-type voltage-gated Ca2+ (CaV2.2) channels, which enable synaptic transmission by triggering neurotransmitter release, are tightly modulated by G protein-coupled receptors (GPCRs) via several downstream signaling messengers, such as Gbg, calmodulin, arachidonic acid and PIP2. However, the molecular mechanism by which Gq/11-coupled receptors (GqPCRs) suppress CaV2.2 currents remains unclear. In this research highlight, we review our recent finding that M1 muscarinic receptors inhibit CaV2.2 channels through both Gbg-mediated voltage-dependent (VD) and Gαq/11/PLC-mediated voltage-independent (VI) pathways. Our photometry results also demonstrate that Gbg-mediated VD inhibition of CaV2.2 channels initiates approximately 3s earlier than VI inhibition, and is strongly potentiated in cells expressing plasma membrane-localized CaV b subunits. Our observations demonstrate a novel mechanism for CaV2.2 channel modulation by GqPCRs where the subcellular location of CaV b subunits plays a critical role in determining the voltage-dependence of current suppression by M1 receptors.
URI
http://hdl.handle.net/20.500.11750/13344
DOI
10.14800/rci.515
Publisher
Smart Science & Technology LLC
Related Researcher
  • Author Suh, Byung-Chang Laboratory of Brain Signal and Synapse Research
  • Research Interests Molecular mechanisms of epilepsy and sensory pain transmission; Signaling mechanism of ion channel regulation and membrane excitability; 분자전기생리; 간질 및 통증의 분자적 기전 연구
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Collection:
Department of Brain SciencesLaboratory of Brain Signal and Synapse Research1. Journal Articles


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