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. 2017 Sep 11;18(11):2015–2029. doi: 10.15252/embr.201643689

Figure EV2. Normal maturation, synapse count, and synaptic function in Lrba mutant IHCs.

Figure EV2

  • A, A′
    Spotlike BK channel (green) staining at the IHC neck region indicates normal IHC maturation in Lrba mutant mice; IHCs have been counterstained for otoferlin (magenta). Scale bar: 5 μm.
  • B, B′
    Synapse count in apical turn IHCs from p14–16 WT and Lrba‐KO mice, as assessed by presynaptic CtBP2 (magenta) and postsynaptic GluA2/3 (green) co‐staining remains unaltered, as quantified in (B′). Data are presented as means ± s.e.m. The dashed line in (B) outlines a single IHC, and asterisks indicate nuclei. Scale bar: 10 μm.
  • C–C″
    Electrophysiologically recorded whole‐cell Ca2+ current–voltage relationship from p14–17 IHCs show similar voltage dependence and current amplitudes in both genotypes. (C′) Exocytic ∆Cm in response to step depolarizations to the respective maximum Ca2+ current potential for either 20 ms (to deplete readily releasable vesicles) or 200 ms (to probe sustained exocytosis) revealed no statistically significant difference in synaptic release between WT (n = 18; N = 16) and Lrba‐KO IHCs (n = 10; N = 7) (P = 0.24 and P = 0.51, respectively; Student's t‐test). (C″) Similarly, release efficiencies for both depolarization durations (i.e., ∆Cm per QCa2+) appear unchanged in Lrba mutants. Data are presented as means ± s.e.m.