The voltage-dependent channels in outer hair cells dissociated from guinea pig cochlea wereinvestigated using a whole-cell patch-clamp technique. Depolarizing voltage steps to potentials morepositive than-30mV elicited a slowly inactivating outward K
+current (I
KCa), which is dependent onintracellular Ca
2+. Hyperpolarizing voltage steps to more negative than-90mV rapidly inactivatedan inward K
+current (Ik, n), which is already activated at resting membrane potential. When both K
+currents were suppressed by replacing K
+ with other cation of large molecule, depolarizing voltagesteps elicited a slowly-inactivating inward current. The maximum values of current amplitudeincreased in a hyperbolic manner with increasing extracellular Ca
2+concentration. Indicating thatouter hair cell possesses L-type Ca
2+channel. The effects of inorganic Ca
2+channel antagonist, which is usually used as drug against systemic circulatory dysfunction, on Ca
2+current in outer haircell were investigated. Inhibitory strength was in the order of flunarizine=nicardipine>=diltiazem.The effects of well-known ototoxic drug, aminoglycoside, on voltage-dependent channels in outerhair cell of guinea pig was examined, because of the easy fragility of outer hair cell to aminoglyocosideantibiotics in the cochlear cells. The aminoglycoside antibiotics selectively suppressed Ca
2+current in outer hair cell. The inhibitory strength was in the order of neomycin>gentamycin≥kanamycin=streptomycin.
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