Outer hair cell (OHC) is widely accepted as the origin of cochlear amplification, a mechanism that accounts for the extreme sensitivity of the mammalian hearing. The key process of cochlear amplification is the reverse transduction, where the OHC changes its length under electrical stimulation. In this study, we developed a method to modulate electro-mechanical transduction with an optogenetic approach based on channelrhodopsin 2 (ChR2), a direct lightactivated non-selective cation channel (NSCC). We specifically expressed ChR2 in mouse cochlea OHCs through in uterus injection of adenovirus vector with ChR2 in fusion with the fluorescent marker tdTomato. We also transfected ChR2(H134R), a point mutant of ChR2, with plasmid to an auditory cell line (HEI-OC1). With whole cell recording, we found that blue light (470 nm) elicited a current with a reversal potential around zero in both mouse OHCs and HEI-OC1 cells and generated depolarization in both cell types.