Intracellular current administration evokes rapid, graded, and bidirectional mechanical responses of isolated outer hair cells from the mammalian inner ear. The cells become shorter in response to depolarizing and longer in response to hyperpolarizing currents in the synaptic end of the cell. The cells respond with either an increase or decrease in length to transcellular alternating current stimulation. The direction of the movement with transcellular stimuli appears to be frequency dependent. Iontophoretic application of acetylcholine to the synaptic end of the cell decreases its length. The microarchitecture of the organ of Corti permits length changes of outer hair cells in a manner that could significantly influence the mechanics of the cochlear partition and thereby contribute to the exquisite sensitivity of mammalian hearing.

https://science.sciencemag.org/content/sci/227/4683/194.full.pdf

Evoked mechanical responses of isolated cochlear outer hair cells

In mammals, environmental sounds stimulate the auditory receptor, the cochlea, via vibrations of the stapes, the innermost of the middle ear ossicles. These vibrations produce displacement waves that travel on the elongated and spirally wound basilar membrane (BM). As they travel, waves grow in amplitude, reaching a maximum and then dying out. The location of maximum BM motion is a function of stimulus frequency, with high-frequency waves being localized to the “base” of the cochlea (near the stapes) and low-frequency waves approaching the “apex” of the cochlea. Thus each cochlear site has a characteristic frequency (CF), to which it responds maximally. BM vibrations produce motion of hair cell stereocilia, which gates stereociliar transduction channels leading to the generation of hair cell receptor potentials and the excitation of afferent auditory nerve fibers. At the base of the cochlea, BM motion exhibits a CF-specific and level-dependent compressive nonlinearity such that responses to low-level, near-CF stimuli are sensitive and sharply frequency-tuned and responses to intense stimuli are insensitive and poorly tuned. The high sensitivity and sharp-frequency tuning, as well as compression and other nonlinearities (two-tone suppression and intermodulation distortion), are highly labile, indicating the presence in normal cochleae of a positive feedback from the organ of Corti, the “cochlear amplifier.” This mechanism involves forces generated by the outer hair cells and controlled, directly or indirectly, by their transduction currents. At the apex of the cochlea, nonlinearities appear to be less prominent than at the base, perhaps implying that the cochlear amplifier plays a lesser role in determining apical mechanical responses to sound. Whether at the base or the apex, the properties of BM vibration adequately account for most frequency-specific properties of the responses to sound of auditory nerve fibers.

/pdf/mechanics-of-the-mammalian-cochlea-368l279klj.pdf

Mechanics of the Mammalian Cochlea

Phantom auditory perception (tinnitus): mechanisms of generation and perception

This paper presents a neurophysiological approach to tinnitus and discusses its clinical implications. A hypothesis of discordant damage of inner and outer hair cells systems in tinnitus generation...

A neurophysiological approach to tinnitus: Clinical implications

Outer hair cell electromotility is a rapid, force generating, length change in response to electrical stimulation. DC electrical pulses either elongate or shorten the cell and sinusoidal electrical stimulation results in mechanical oscillations at acoustic frequencies. The mechanism underlying outer hair cell electromotility is thought to be the origin of spontaneous otoacoustic emissions. The ability of the cell to change its length requires that it be mechanically flexible. At the same time the structural integrity of the organ of Corti requires that the cell possess considerable compressive rigidity along its major axis. Evolution appears to have arrived at novel solutions to the mechanical requirements imposed on the outer hair cell. Segregation of cytoskeletal elements in specific intracellular domains facilitates the rapid movements. Compressive strength is provided by a unique hydraulic skeleton in which a positive hydrostatic pressure in the cytoplasm stabilizes a flexible elastic cortex with circumferential tensile strength. Cell turgor is required in order that the pressure gradients associated with the electromotile response can be communicated to the ends of the cell. A loss in turgor leads to loss of outer hair cell electromotility. Concentrations of salicylate equivalent to those that abolish spontaneous otoacoustic emissions in patients weaken the outer hair cell's hydraulic skeleton. There is a significant diminution in the electromotile response associated with the loss in cell turgor. Aspirin's effect on outer hair cell electromotility attests to the role of the outer hair cell in generating otoacoustic emissions and demonstrates how their physiology can influence the propagation of otoacoustic emissions.

/pdf/outer-hair-cell-electromotility-and-otoacoustic-emissions-174onlvisu.pdf

Jonathan H. Siegel

Papers

Efferent neural control of cochlear mechanics? Olivocochlear bundle stimulation affects cochlear biomechanical nonlinearity.