ePoster

ATP INDUCED CA<SUP>2+</SUP> TRANSIENTS INFLUENCED BY THE TONOTOPICAL LOCATION IN THREE GLIA-LIKE SUPPORTING CELLS IN THE HEARING ORGAN

Eszter Berekmériand 5 co-authors

University of Veterinary Medicine Budapest

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-662

Presentation

Date TBA

Board: PS03-08AM-662

Poster preview

ATP INDUCED CA<SUP>2+</SUP> TRANSIENTS INFLUENCED BY THE TONOTOPICAL LOCATION IN THREE GLIA-LIKE SUPPORTING CELLS IN THE HEARING ORGAN poster preview

Event Information

Poster Board

PS03-08AM-662

Abstract

Physiology and pathophysiology of cochlear supporting cells are studied mostly in newborn rodents. Mice and rats born deaf and significant postnatal development needed cells to be able to be activated by external sound sources. The presence of purinergic receptors and the changes in the expression profile during the development have been demonstrated in the cochlea. Supporting cells’ ATP activated receptors have role in the maturation of synapses between receptor cells, however, the adult receptor pattern is still sparse.
We have examined the Claudius’, Hensen’s and Deiters’ cells of BALB/c mice, older than 14 days. Hemicochlea preparation and single-cell electroporation with Ca2+ sensitive dye let us investigate the differences of the ATP induced Ca2+ transients.
The characteristics of the transients (amplitude, duration and area under curves) were collected in three turns of the cochlea. Based on the experimental data we set up a mathematical model to explore the detailed mechanisms involved in the Ca2+ concentration elevation and removing of the excess ions.
Experimental and model results suggest elementary differences between the three measured supporting cells’ Ca2+ handling mechanism: parameters of Ca2+ removing mechanism (especially in parameters of sarco-/endoplasmic Ca2+/ATP-ase function) and the ionotropic P2X receptors have the biggest differences among the cells. The tonotopy influenced both the Ca2+ entrance into the cytoplasm and the removal of it. According to our model new experiments could be designed to decipher the precise role of the intracellular Ca2+ regulation in supporting cells in the function of hearing and hearing sensitivity.

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