Gap junction-mediated intercellular biochemical coupling in cochlear supporting cells is required for normal cochlear functions.

ABSTRACT: Dysfunction of gap junctions (GJs) caused by mutations in connexin26 (Cx26) and Cx30 accounts for nearly half of all cases of hereditary nonsyndromic deafness cases. Although it is widely held that GJs connecting supporting cells in the organ of Corti mainly provide ionic pathways for rapid removal of K+ around the base of hair cells, the function of GJs in the cochlea remains unknown. Here we show that GJs were not assembled in the supporting cells of the organ of Corti until 3 days after birth in mice and then gradually matured to connect supporting cells before the onset of hearing. In organotypic cochlear cultures that were confirmed to express GJs, GJs mediated the propagation of intracellular Ca2+ concentration waves in supporting cells by allowing intercellular diffusion of inositol

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC1257692 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature