Abstract
Signal transmission by sensory auditory and vestibular hair cells relies upon Ca(2+)-dependent exocytosis of glutamate. The Ca(2+) current in mammalian inner ear hair cells is predominantly carried through Ca (V) 1.3 voltage-gated Ca(2+) channels. Despite this, Ca (V) 1.3 deficient mice (Ca (V) 1.3(-/-) ) are deaf but do not show any obvious vestibular phenotype. Here, we compared the Ca(2+) current (I (Ca) ) in auditory and vestibular hair cells from wild-type and Ca (V) 1.3(-/-) mice, to assess whether differences in the size of the residual I (Ca) could explain, at least in part, the two phenotypes. Using 5 mM extracellular Ca(2+) and near-body temperature conditions, we investigated the cochlear primary sensory receptors inner hair cells (IHCs) and both type I and type II hair cells of the semicircular canals. We found that the residual I (Ca) in both auditory and vestibular hair cells from Ca (V) 1.3(-/-) mice was less than 20% (12-19%, depending on the hair cell type and age investigated) compared to controls, indicating a comparable expression of Ca (V) 1.3 Ca(2+) channels in both sensory organs. We also showed that, different from IHCs, type I and type II hair cells from Ca (V) 1.3(-/-) mice were able to acquire the adult-like K(+) current profile in their basolateral membrane. Intercellular K(+) accumulation was still present in Ca (V) 1.3(-/-) mice during I (K,L) activation, suggesting that the K(+)-based, non-exocytotic, afferent transmission is still functional in these mice. This non-vesicular mechanism might contribute to the apparent normal vestibular functions in Ca (V) 1.3(-/-) mice.