Journal
ISCIENCE
Volume 25, Issue 12, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2022.105628
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Categories
Funding
- Fondation Pour l'Audition [FPA IDA05, FPA IDA03, FPA IDA08]
- DIM Ile de France
- EARGENCURE [ANR-17-CE18-0027]
- RHUAUDINNOVE [ANR-18-RHUS-0007]
- Agence Nationale de la Recherche (ANR) [ANR-17-CE18-0027, ANR-18-RHUS-0007] Funding Source: Agence Nationale de la Recherche (ANR)
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This study found that SNAP-25 is essential for normal hearing function by ensuring exocytosis and maintenance of ribbon synapses in IHCs.
Hearing depends on fast and sustained calcium-dependent synaptic vesicle fusion at the ribbon synapses of cochlear inner hair cells (IHCs). The implication of the canonical neuronal SNARE complex in this exocytotic process has so far remained controversial. We investigated the role of SNAP-25, a key component of this complex, in hearing, by generating and analyzing a conditional knockout mouse model allowing a targeted postnatal deletion of Snap-25 in IHCs. Mice subjected to IHC Snap-25 inactivation after hearing onset developed severe to profound deafness because of defective IHC exocytosis followed by ribbon degeneration and IHC loss. Viral transfer of Snap-25 in these mutant mice rescued their hearing function by restoring IHC exocytosis and preventing synapses and hair cells from degeneration. These results demonstrate that SNAP-25 is essential for normal hearing function, most likely by ensuring IHC exocytosis and ribbon synapse maintenance.
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