Abstract
The reticular lamina of the mammalian cochlea is formed by the tightly joined apical surfaces of hair cells and supporting cells. This lamina creates a barrier separating endolymph and perilymph, two fluids of different composition. The preservation of this fluid barrier is a requirement for cochlear function. This study aimed to determine whether the calcium-dependent, cell adhesion molecule, E-cadherin was appropriately placed both temporally and spatially to contribute to the formation and maintenance of the reticular lamina. Cochleas aged E15 to P31 were stained immunocytochemically for E-cadherin. In the P31 organ of Corti, E-cadherin is localized to the apical intercellular junctions of supporting cells, but is absent from supporting cell-hair cell borders. During development, E-cadherin is present only on the apices and lateral edges of those cells which will eventually lie adjacent to fluid spaces — pillar, outer hair and Deiters cells. The molecule disappears from the lateral cell membranes at about the time in development that fluid spaces form. These data suggest that E-cadherin plays a role in maintaining the reticular lamina by mediating inter-supporting cell adhesion and raise the possibility that fluid space opening in the organ of Corti is facilitated by the down-regulation or redistribution of E-cadherin.