Abstract:
:We studied the role of the synaptic ribbon for sound encoding at the synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in mice lacking RIBEYE (RBEKO/KO). Electron and immunofluorescence microscopy revealed a lack of synaptic ribbons and an assembly of several small active zones (AZs) at each synaptic contact. Spontaneous and sound-evoked firing rates of SGNs and their compound action potential were reduced, indicating impaired transmission at ribbonless IHC-SGN synapses. The temporal precision of sound encoding was impaired and the recovery of SGN-firing from adaptation indicated slowed synaptic vesicle (SV) replenishment. Activation of Ca2+-channels was shifted to more depolarized potentials and exocytosis was reduced for weak depolarizations. Presynaptic Ca2+-signals showed a broader spread, compatible with the altered Ca2+-channel clustering observed by super-resolution immunofluorescence microscopy. We postulate that RIBEYE disruption is partially compensated by multi-AZ organization. The remaining synaptic deficit indicates ribbon function in SV-replenishment and Ca2+-channel regulation.
journal_name
Elifejournal_title
eLifeauthors
Jean P,Lopez de la Morena D,Michanski S,Jaime Tobón LM,Chakrabarti R,Picher MM,Neef J,Jung S,Gültas M,Maxeiner S,Neef A,Wichmann C,Strenzke N,Grabner C,Moser Tdoi
10.7554/eLife.29275subject
Has Abstractpub_date
2018-01-12 00:00:00issn
2050-084Xpii
29275journal_volume
7pub_type
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