When illuminated by an ultraviolet laser, a newly developed photonic drug has been shown to inactivate prestin, a motor protein in the ear, revealing how the cochlea amplifies sound. The inner ear actively amplifies sound from forces generated by outer hair cells in the cochlea, but exactly how it accomplishes this had always been somewhat of a mystery. The new technique, developed by Dr. Jonathan A.N. Fisher and colleagues at The Rockefeller University, reveals how the cochlea actively self-amplifies sound it receives to help increase the range of sounds that can be heard. The team accomplished this by inactivating the motor protein involved in the movement of the outer hair cells — the true sensory cells of the inner ear. Sound waves traveling down the cochlea produce actual waves that can be observed along the basilar membrane, the tissue that lines the interior of the bony cochlea. Various sound frequencies along its length can be picked up by the cochlea, with higher frequency sounds picked up at the center of the “snail” and the lower frequency sounds being picked up at the part of the cochlea closest to the eardrum. The outer hair cells have been known to provide amplification of sound waves picked up by the inner hair cells by actively changing their shape to increase the amplitudes of the sound waves. The outer hair cells can do this because the membrane protein can contract and cause the stereocillia to be deflected by the overlying tectorial membrane. Using the drug, the scientists affected prestin at very specific locations along the basilar membrane. By inactivating the protein at certain points, the sound-evoked waves that carry mechanical signals to sensory hair cells were reshaped and of smaller amplitude, indicating that, without prestin, amplification is dampened compared with when the protein was allowed to function normally. Their findings reveal how prestin’s molecular forces pump energy into the waves within the cochlea and how this energy is pushed forward as the wave travels. The research, published in Neuron (doi: 10.1016/j.neuron.2012.09.031), was supported by a grant from the American Hearing Research Foundation. For more information, visit: www.rockefeller.edu