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Coordinated calcium signalling in cochlear sensory and non‐sensory cells refines afferent innervation of outer hair cells
Author(s) -
Ceriani Federico,
Hendry Aenea,
Jeng JingYi,
Johnson Stuart L,
Stephani Friederike,
Olt Jennifer,
Holley Matthew C,
Mammano Fabio,
Engel Jutta,
Kros Corné J,
Simmons Dwayne D,
Marcotti Walter
Publication year - 2019
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201899839
Subject(s) - sensory system , biology , ribbon synapse , cochlea , neuroscience , afferent , inner ear , sensory receptor , hair cell , calcium signaling , calcium imaging , receptor , signalling , calcium , microbiology and biotechnology , anatomy , signal transduction , medicine , vesicle , biochemistry , membrane , synaptic vesicle , genetics
Outer hair cells (OHCs) are highly specialized sensory cells conferring the fine‐tuning and high sensitivity of the mammalian cochlea to acoustic stimuli. Here, by genetically manipulating spontaneous Ca 2+ signalling in mice in vivo, through a period of early postnatal development, we find that the refinement of OHC afferent innervation is regulated by complementary spontaneous Ca 2+ signals originating in OHCs and non‐sensory cells. OHCs fire spontaneous Ca 2+ action potentials during a narrow period of neonatal development. Simultaneously, waves of Ca 2+ activity in the non‐sensory cells of the greater epithelial ridge cause, via ATP‐induced activation of P2X 3 receptors, the increase and synchronization of the Ca 2+ activity in nearby OHCs. This synchronization is required for the refinement of their immature afferent innervation. In the absence of connexin channels, Ca 2+ waves are impaired, leading to a reduction in the number of ribbon synapses and afferent fibres on OHCs. We propose that the correct maturation of the afferent connectivity of OHCs requires experience‐independent Ca 2+ signals from sensory and non‐sensory cells.