Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 44, Issue 3, Pages 246-259Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2010.03.011
Keywords
Calcium channels; Channel gating; Calcium current inactivation; Inner hair cells; Hearing
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Funding
- Marie Curie Research Training Network CavNET [MRTN-CT-2006-035367]
- Austrian Science Funds [P20760]
- University of Innsbruck (Austria)
- Austrian Science Fund (FWF) [P 20670] Funding Source: researchfish
- Austrian Science Fund (FWF) [P20760] Funding Source: Austrian Science Fund (FWF)
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Neurotransmitter release and spontaneous action potentials during cochlear inner hair cell (IHC) development depend on the activity of Ca(v)1.3 voltage-gated L-type Ca2+ channels. Their voltage- and Ca2+-dependent inactivation kinetics are slower than in other tissues but the underlying molecular mechanisms are not yet understood. We found that Rab3-interacting molecule-2 alpha (RIM2 alpha) mRNA is expressed in immature cochlear IHCs and the protein co-localizes with Ca(v)1.3 in the same presynaptic compartment of IHCs. Expression of RIM proteins in tsA-201 cells revealed binding to the beta-subunit of the channel complex and RIM-induced slowing of both Ca2+- and voltage-dependent inactivation of Ca(v)1.3 channels. By inhibiting inactivation, RIM induced a non-inactivating current component typical for IHCCa(v)1.3 currents which should allow these channels to carry a substantial window current during prolonged depolarizations. These data suggest that RIM2 contributes to the stabilization of Ca(v)1.3 gating kinetics in immature IHCs. (C) 2010 Elsevier Inc. All rights reserved.
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