The sense of hearing in mammals is uniquely sensitive, capable of discerning a vast range of sound intensities and frequencies. This remarkable ability is largely thanks to a specialized motor protein called prestin. Named after the musical term “presto” to signify its incredibly fast action, prestin functions as a microscopic engine within the inner ear. It drives the mechanical amplification of sound, allowing for the perception of faint noises that would otherwise be lost.
Its absence or malfunction leads to a significant loss of hearing sensitivity. This molecular machine represents a key evolutionary development for high-frequency hearing in mammals.
The Location and Function of Prestin in the Inner Ear
Deep within the spiral-shaped cochlea of the inner ear reside specialized sensory cells known as outer hair cells (OHCs). These cells are distinct from the inner hair cells, which are responsible for sending auditory signals to the brain. The primary role of the OHCs is not to send signals, but to physically amplify sound vibrations. Prestin is almost exclusively found densely packed within the lateral plasma membrane of these OHCs, the very region where their movement originates.
Its presence enables the OHCs to act like tiny, fast-acting pistons. When stimulated, the prestin proteins collectively change their shape, causing the entire OHC to elongate and contract. This physical movement, known as electromotility, is the core function of the OHCs. The expression pattern of prestin directly correlates with the appearance of this electromotile capability in developing mammals, underscoring its direct role in this mechanical function.
The Mechanism of Electromotility
The process of hearing begins when sound waves are converted into electrical signals within the cochlea. Prestin’s unique function is to act as a direct voltage-to-movement converter. The protein is a member of the SLC26A family of solute carriers, but unlike its relatives that transport ions, prestin has evolved to use changes in membrane voltage to generate force. This capability is the foundation of somatic electromotility.
When a sound wave stimulates the ear, the electrical potential across the OHC’s membrane fluctuates. In response to these voltage changes, each prestin protein undergoes a conformational change, altering its surface area. This molecular shape-shifting is extraordinarily rapid, allowing the protein to keep pace with the frequencies of incoming sounds. The collective action of millions of prestin molecules changing shape in unison forces the entire cell to lengthen and shorten. This cycle of contraction and elongation occurs at speeds that match the incoming sound frequencies, reaching thousands of times per second for high-pitched sounds.
How Prestin Amplifies Sound
The rapid, voltage-driven movement of the outer hair cells is the driving force behind the cochlear amplifier. This amplification process is what provides mammals with their exceptional hearing sensitivity and the ability to distinguish between closely related frequencies. The electromotility of the OHCs does not directly send a signal to the brain but instead creates a positive feedback loop within the cochlea.
As the OHCs lengthen and shorten in time with a sound wave, they push and pull on the surrounding structures and fluids of the inner ear. This mechanical action effectively boosts the vibration, particularly for low-intensity sounds. The added energy from the OHCs’ movement makes the vibration stronger, which in turn leads to a greater stimulation of the inner hair cells—the cells that actually transmit the auditory signal to the brain.
Prestin’s Role in Hearing Disorders
Defects in prestin can lead to significant hearing impairment. The protein is encoded by the SLC26A5 gene, and mutations are a known cause of non-syndromic sensorineural hearing loss, characterized by damage to the hair cells. Individuals with mutations affecting prestin lose the benefit of the cochlear amplifier. This results in a substantial decrease in hearing sensitivity, making it difficult to perceive quiet sounds and discriminate between different frequencies.
Studies on mouse models where the prestin gene has been altered confirm its role; these mice exhibit a complete loss of OHC electromotility and a hearing sensitivity loss of up to 60 dB. The targeted nature of prestin’s function makes it a subject of interest for future therapies. Because damage to OHCs is often permanent, research is exploring ways to protect these cells or restore their function, including gene therapy approaches aimed at correcting the defective SLC26A5 gene.