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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.

Inhibition of K+outward currents by linopirdine in the cochlear outer hair cells of circling mice within the first postnatal week