gms | German Medical Science

Introduction: Gap junctions are specialised plasma membrane regions between adjoining metazoen cells. They provide the exchange of ions and small molecules or energy metabolites, thus regulating the metabolic and electrical status of a cellular syncytium. In the mammalian cochlea, Hensen cells are the major population of supporting cells. They are coupled by gap junctions predominantly composed of Connexin 26 (Cx26). Mutations of genes encoding for Cx26 account for the majority of non syndomatic hearing loss.

Material and Methods: Using the double whole-patch clamp technique gap junctional conductance was measured in isolated Hensen-cells of guinea pig cochlea. Regulation of gap junctional coupling was determined by applying different intracellular ATP-concentrations and ATP-dependent K+-channel blockers.

Results: Intracellular ATP regulates gap junctional coupling of isolated Hensen cells of guinea pig in a dose dependent manner. The effect of ATP could be mimicked by replacement of ATP in the pipette filling solution by a non-hydrolysable analogue. The results indicate that ATP-dependent K+-channels are involved in the regulation of gap junction coupling independently of ATP hydrolysis in phosphorylation processes or transduction pathways. It is proposed that in Hensen cells gap junctional coupling related to the permeability of ATP-sensitive K+ channels acts via a Ca2+- and voltage -independent mechanism.

Conclusion: Interacting transport mechanism of ATP-dependent K+-channels and cell-to-cell channels in Hensen cells may play an important role in spatial buffering of K+, that is released by sensory cells upon sound stimulation, thereby preventing toxic extracellular accumulation as well as for the K+ efflux to the endolymph and the maintenance of the endocochlear potential.