Abstract
Native Ca V1.3 channels within cochlear hair cells exhibit a surprising lack of Ca 2+-dependent inactivation (CDI), given that heterologously expressed Ca V1.3 channels show marked CDI. To determine whether alternative splicing at the C terminus of the Ca V1.3 gene may produce a hair cell splice variant with weak CDI, we transcript-scanned mRNA obtained from rat cochlea. We found that the alternate use of exon 41 acceptor sites generated a splice variant that lost the calmodulin-binding IQ motif of the C terminus. These Ca V1.3 IQΔ ("IQ deleted") channels exhibited a lack of CDI, which was independent of the type of coexpressed β-subunits. Ca V1.3 IQΔ channel immunoreactivity was preferentially localized to cochlear outer hair cells (OHCs), whereas that of Ca V1.3 IQfull channels (IQ-possessing) labeled inner hair cells (IHCs). The preferential expression of Ca V1.3 IQΔ within OHCs suggests that these channels may play a role in processes such as electromotility or activity-dependent gene transcription rather than neurotransmitter release, which is performed predominantly by IHCs in the cochlea.
Original language | English (US) |
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Pages (from-to) | 10690-10699 |
Number of pages | 10 |
Journal | Journal of Neuroscience |
Volume | 26 |
Issue number | 42 |
DOIs | |
State | Published - Oct 18 2006 |
Keywords
- Alternative splicing
- Calcium channels
- Calcium-dependent inactivation
- Hair cells
- L-type calcium channels
- Splice variant
ASJC Scopus subject areas
- Neuroscience(all)