Gentamicin's Influence On The Electrophysiological Properties Of Acutely Dissociated Murine Coclear Spiral Ganglion Neurons

Objective: To explore the influence of gentamicin on acutely dissociated murine coclear spiral ganglion neurons' electrophysiological properties and its significance.Method: Murine coclear spiral ganglion neurons ( SGN) were dissociated acutely using trypsin. Indirect immunocytochemical identification was performed and cells were observed under fluorescent microscope. Potassium and sodium channel currents of acutely trypsin-dissociated spiral ganglion neurons were recorded and analyzed, using whole-cell variation of the voltage clamp technique. We studied gentamicin's influence on the peak currents of potassium and sodium channels on cell membranes of spiral ganglion neurons, and the relationship to gentamicin's concentration in extracellular fluid, and the currents' recovery after gentamicin being washed out.Results: The light-green cells under fluorescent microscope were spiral ganglion neurons. In the membranes of spiral ganglion neurons, we recordedtetraethylammonium chloride (TEA-C1) -sensitive and 4-aminopyridine (4-AP) -sensitive outside delayed rectifier potassium currents and A-type potassium currents, and tetrodotoxin (TTX) -sensitive inside sodium currents. Ion channels' activities had the character of voltage-dependence. Gentamicin could inhibit voltage-dependent potassium channels, but it couldn't inhibit voltage-dependent sodium channels. Gentamicin's inhibitation on potassium currents had dose-dependence on gentamicin's concemtration in extracellular fluid and the currents recoverd incompletely after gentamicin being washed out.Conclusion: The electrophysiological properties of acutely dissociated SGN were the important reference to the research of the mechanics of auditory propagation. There were mainly delayed rectifier potassium channel, A-type potassium channel and sodium channel on cell membranes of acutely dissociated spiral ganglion neurons. And this research explained the ototoxic mechanism of gentamicin through its action on keeping from SGN' potassium channels from the electrophysiological aspect.