ArticleProceedings of the National Academy of Sciences of the United States of America2015
Rab3-interacting molecules 2α and 2β promote the abundance of voltage-gated CaV1.3 Ca2+ channels at hair cell active zones.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 77 citations in OpenAlex.
- The missing link: Piccolino is essential for tethering synaptic vesicles to rod photoreceptor ribbons.The Journal of cell biology · 2026Article
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- Charting the nanotopography of inner hair cell synapses using MINFLUX nanoscopy.Science advances · 2025Article
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
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- On the targeting of voltage-gated calcium channels to neurotransmitter release sites.Current opinion in neurobiology · 2024Review
- CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Diversity matters - extending sound intensity coding by inner hair cells via heterogeneous synapses.The EMBO journal · 2023Review
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- Piccolino is required for ribbon architecture at cochlear inner hair cell synapses and for hearing.EMBO reports · 2023Article
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- Synaptic activity is not required for establishing heterogeneity of inner hair cell ribbon synapses.Frontiers in molecular neuroscience · 2023Article
- Probing the role of the CFrontiers in molecular neuroscience · 2023Article
- Optogenetics and electron tomography for structure-function analysis of cochlear ribbon synapses.eLife · 2022Article
- The SNARE protein SNAP-25 is required for normal exocytosis at auditory hair cell ribbon synapses.iScience · 2022Article
- Resolving the molecular architecture of the photoreceptor active zone with 3D-MINFLUX.Science advances · 2022Article
- Circular RNAs: Emblematic Players of Neurogenesis and Neurodegeneration.International journal of molecular sciences · 2022Review
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- RIM-Binding Protein 2 Organizes CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Encoding sound in the cochlea: from receptor potential to afferent discharge.The Journal of physiology · 2021Review
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Authors and funding
16 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) influx triggers the fusion of synaptic vesicles at the presynaptic active zone (AZ). Here we demonstrate a role of Ras-related in brain 3 (Rab3)-interacting molecules 2α and β (RIM2α and RIM2β) in clustering voltage-gated CaV1.3 Ca(2+) channels at the AZs of sensory inner hair cells (IHCs). We show that IHCs of hearing mice express mainly RIM2α, but also RIM2β and RIM3γ, which all localize to the AZs, as shown by immunofluorescence microscopy. Immunohistochemistry, patch-clamp, fluctuation analysis, and confocal Ca(2+) imaging demonstrate that AZs of RIM2α-deficient IHCs cluster fewer synaptic CaV1.3 Ca(2+) channels, resulting in reduced synaptic Ca(2+) influx. Using superresolution microscopy, we found that Ca(2+) channels remained clustered in stripes underneath anchored ribbons. Electron tomography of high-pressure frozen synapses revealed a reduced fraction of membrane-tethered vesicles, whereas the total number of membrane-proximal vesicles was unaltered. Membrane capacitance measurements revealed a reduction of exocytosis largely in proportion with the Ca(2+) current, whereas the apparent Ca(2+) dependence of exocytosis was unchanged. Hair cell-specific deletion of all RIM2 isoforms caused a stronger reduction of Ca(2+) influx and exocytosis and significantly impaired the encoding of sound onset in the postsynaptic spiral ganglion neurons. Auditory brainstem responses indicated a mild hearing impairment on hair cell-specific deletion of all RIM2 isoforms or global inactivation of RIM2α. We conclude that RIM2α and RIM2β promote a large complement of synaptic Ca(2+) channels at IHC AZs and are required for normal hearing.
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