Activation of TRPC4 beta by G alpha(i) subunit increases Ca2+ selectivity and controls neurite morphogenesis in cultured hippocampal neuron
- Authors
- Jeon, Jae-Pyo; Roh, Seung-Eon; Wie, Jinhong; Kim, Jinsung; Kim, Hana; Lee, Kyu-Pil; Yang, Dongki; Jeon, Ju-Hong; Cho, Nam-Hyuk; Kim, In-Gyu; Kang, David E.; Kim, Hyun Jin; So, Insuk
- Issue Date
- Oct-2013
- Publisher
- CHURCHILL LIVINGSTONE
- Keywords
- TRPC; Transient receptor potential channel; TRPC4; Galphai2; Gi2; Dendrite; Neurite; Calcium
- Citation
- CELL CALCIUM, v.54, no.4, pp.307 - 319
- Journal Title
- CELL CALCIUM
- Volume
- 54
- Number
- 4
- Start Page
- 307
- End Page
- 319
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/14247
- DOI
- 10.1016/j.ceca.2013.07.006
- ISSN
- 0143-4160
- Abstract
- The ubiquitous transient receptor potential canonical (TRPC) channels function as non-selective, Ca2+-permeable channels. TRPC channels are activated by stimulation of Gag-PLC-coupled receptors. Here, we report that TRPC4/TRPC5 can be activated by G alpha(i). We studied the essential role of G alpha(i), subunits in TRPC4 activation and investigated changes in ion selectivity and pore dilation of the TRPC4 channel,elicited by the G alpha(i2) subunit. Activation of TRPC4 by Gam increased Ca2+ permeability and Ca2+ influx through TRPC4 channels. Co-expression of the muscarinic receptor (M2) and TRPC4 in HEK293 cells induced TRPC4-mediated Ca2+ influx. Moreover, both TRPC4 beta and the TRPC4 beta-G alpha(12) signaling complex induced inhibition of neurite growth and arborization in cultured hippocampal neurons. Cells treated with KN-93, a CaMKII inhibitor, prevented TRPC4- and TRPC4-G alpha(Q205L)(12)-mediated inhibition of neurite branching and growth. These findings indicate an essential role of G alpha(i) proteins in TRPC4 activation and extend our knowledge of the functional role of TRPC4 in hippocampal neurons. (C) 2013 Elsevier Ltd. All rights reserved.
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