. 2007 Mar 21;27(12):3163–3173. doi: 10.1523/JNEUROSCI.3974-06.2007

Table 2.

Comparison of developmental IHC defects in mutants with TH signaling defects in comparison to Ca_V1.3 knock-out and Tmc1 mutants

	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 reduced^a ^b, 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 defect^c ^d	BK and KCNQ₄ not detectable up to P58	Only few nerve endings found at P15	Maintained immature Ca²⁺ current and exocytosis	Not evaluated
Ca_V1.3 deletion^e ^f	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 Ca_V1.3^−/− mice. Common phenotypes are in bold.

^aRusch et al., 1998.

^bRusch et al., 2001.

^cBock and Steel, 1983.

^dMarcotti et al., 2006.

^eBrandt et al., 2003.

^fNemzou et al., 2006.