Inhibition of K+ outward currents by linopirdine in the outer hair cells (OHCs) of circling mice (homozygous (cir /cir ) mice), an animal model for human deafness (DFNB6 type), was investigated using a whole cell patch clamp technique. Littermate heterozygous (+/cir ) and ICR mice of the same age (postnatal day (P) 0 –P6) were used as controls. Voltage steps from –100 mV to 40 mV elicited small inward currents (–100 mV~–70 mV) and slow rising K+ outward currents (–60 mV ~40 mV) which activated near –50 mV in all OHCs tested. Linopirdine, a known blocker of K+ currents activated at negative potentials (I K,n), did cause inhibition at varying degree (severe, moderate, mild) in K+ outward currents of heterozygous (+/cir ) or homozygous (cir /cir ) mice OHCs in the concentration range between 1 and 100 μM, while it was apparent only in one ICR mice OHC out of nine OHCs at 100 μM. Although the half inhibition concentrations in heterozygous (+/cir ) or homozygous (cir /cir ) mice OHCs were close to those reported in I K,n, biophysical and pharmacological properties of K+ outward currents, such as the activation close to –50 mV, small inward currents evoked by hyperpolarizing steps and TEA sensitivity, were not in line with I K,n reported in other tissues. Our results show that the delayed rectifier type K+ outward currents, which are not similar to I K,n with respect to biophysical and pharmacological properties, are inhibited by linopirdine in the developing (P0~P6) homozygous (cir /cir ) or heterozygous (+/cir ) mice OHCs.