Acquisition of BK and KCNQ4 current | Ribbon synapse morphology | Ribbon synapse function (Ca2+ current and exocytosis) | Efferent IHC innervation | |
---|---|---|---|---|
TH signaling defect | BK delayed and reducedab, BK and KCNQ4 not detectable up to P15 in Pax8 KO | Retarded synaptogenesis in Pax8 knock-outs | Late upregulation and no maturation at least up to P15 in Pax8 knock-outs | Maintained at least up to P15 in Pax8 knock-outs |
Tmc1 defectcd | BK and KCNQ4 not detectable up to P58 | Only few nerve endings found at P15 | Maintained immature Ca2+ current and exocytosis | Not evaluated |
CaV1.3 deletionef | BK not detectable up to P35; KCNQ4 present | Normal synaptogenesis, secondary loss | Stimulus–secretion coupling blocked; normal exocytosis during Ca2+ uncaging | Maintained at least up to P45 |
The table compares the developmental abnormalities of hair cells and their synapses between hypothyroid mutants, Tmc1 mutants, and CaV1.3−/− mice. Common phenotypes are in bold.