To overcome the wide-spread electrical neural excitation associated with electrical cochlear implants (eCI), stimulation of spiral ganglion neurons (SGNs) using light presents an attractive solution, as light can be better confined in space. Using optogenetics, SGNs are rendered light sensitive following a viral delivery of a Channelrhodopsin (ChR) transgene to the cochlea. Our group has provided in vivo evidence to support the clinical potential of the optical CI, but for clinical translation, it is critical to optimize individual components of the gene therapy. To this end, we have employed different rodent models of deafness to investigate the preclinical efficacy of this therapy. Adeno-associated virus carrying ChR transgenes were introduced to cochleae of adult kanamycin-deafened Mongolian gerbils using a microcatheter inserted into the round window (RW) with a vent at the stapedial footplate; and to transgenic Otoferlin-KO mice (Otoftm1.1Erei) at post-natal day 6 using pressure injection through the RW. After 4 to 6 weeks, a laser-coupled fiber (594, 522, or 660 nm) was inserted into the RW and optically evoked auditory brainstem recordings (oABR) were measured. Subsequently, cochleae were extracted for immunohistological analysis. Preliminary results show that kanamycin deafening produced a shift in acoustic ARB threshold of at least 50 dB SPL in adult gerbils. Notably, one ChR (ChReef) exhibited high oABR amplitudes of 8 to 15 μV and low energy thresholds (170 nJ) during optical stimulations of 1 ms at 20 Hz. Thus, ChReef shows great promise for the future development of the oCI and other optogenetic applications.