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By Jochen Schacht, Richard R. Fay

The prior decade has introduced nice advances in our realizing of the mechanisms underlying auditory pathologies. This quantity offers fresh advancements in study and their power translation to the scientific atmosphere. It brings jointly the fundamental and scientific sciences very properly in that whereas so much chapters are written by way of simple scientists, every one subject has a beautiful direct scientific software or implication.

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Extra resources for Auditory Trauma, Protection, and Repair (Springer Handbook of Auditory Research)

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1998). 2. 2 Connexin 30 Connexin 30 is the protein product of the GJB6 gene, which lies within the same genetic interval of GJB2 gene, DFNB1. It presents a similar expression configuration in the inner ear as connexin 26. A 342-kb deletion in the GJB6 gene is directly linked to recessive NSHL (Lerer et al. 2001; del Castillo et al. 2002). The deletion was initially identified when an unusually larger number of profoundly deaf individuals with only one GJB2 mutation were documented, more than expected given the carrier rate of GJB2 mutations in the general population.

Hirschfield. References Adato A, Vreugde S, Joensuu T, Avidan N, Hamalainen R, Belenkiy O, Olender T, Bonne-Tamir B, Ben-Asher E, Espinos C, Mill·n JM, Lehesjoki A-E, Flannery JG, Avraham KB, Pietrokovski S, Sankila E-M, Beckmann JS, Lancet D (2002) USH3A transcripts encode clarin-1, a four-transmembrane-domain protein with a possible role in sensory synapses. Eur J Hum Genet 10:339–350. Adato A, Michel V, Kikkawa Y, Reiners J, Alagramam KN, Weil D, Yonekawa H, Wolfrum U, El-Amraoui A, Petit C (2005) Interactions in the network of Usher syndrome type 1 proteins.

The most accepted theory regarding the role of connexin 26 in the inner ear is that it propagates the recycling of potassium ions necessary for the transmission of the auditory signal within hair cells, through gap junctions situated between supporting cells. This way, rapid circulation of potassium ions back to the endolymph through the stria vascularis (Kikuchi et al. 1995; Forge et al. 1999), allows maintenance of a high cochlear potential. The above hypothesis is based on the expression profile of connexin 26 in the cochlea, which is markedly noticeable in the bulky gap junctions of supporting cells of the sensory hair cells of the cochlea, the spiral ligament and in the spiral limbus (Kikuchi et al.

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