The synaptic ribbon is critical for sound encoding at high rates and with temporal precision. Jean, P., Lopez de la Morena, D., Michanski, S., Jaime Tobón, L. M., Chakrabarti, R., Picher, M. M., Neef, J., Jung, S., Gültas, M., Maxeiner, S., Neef, A., Wichmann, C., Strenzke, N., Grabner, C., & Moser, T. eLife, 7:e29275, 2018.
The synaptic ribbon is critical for sound encoding at high rates and with temporal precision [link]Paper  doi  abstract   bibtex   
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.
@article{Jean,
	title = {The synaptic ribbon is critical for sound encoding at high rates and with temporal precision},
	volume = {7},
	issn = {2050-084X},
	url = {https://elifesciences.org/articles/29275},
	doi = {10.7554/eLife.29275},
	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 = {eLife},
	author = {Jean, Philippe and Lopez de la Morena, David and Michanski, Susann and Jaime Tobón, Lina María and Chakrabarti, Rituparna and Picher, Maria Magdalena and Neef, Jakob and Jung, SangYong and Gültas, Mehmet and Maxeiner, Stephan and Neef, Andreas and Wichmann, Carolin and Strenzke, Nicola and Grabner, Chad and Moser, Tobias},
	year = {2018},
	pages = {e29275},
}

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