Taking off a bit on last week’s controversy between Thomas Gold and Georg von Bekesy , rivals on their respective sides of the argument of passive versus resonance theories of  cochlear mechanics.  While researching last week’s Hearing International,  I came across an interesting discussion of hair cell electromotility.   Recall that the predominate cochlear mechanics theory of the 1950s, 1960s and for part of the 1970s was the passive theory while, since 1978 and the discovery of otoacoustic emissions  (OAE), the resonance theory has become the current thought on cochlear mechanics.  While the OAE was known, OAE generator sites were yet to be proven.  Electomotility of the outer hair cells was thought to be the generator for the OAE but it was up to Brownell and colleagues to actually demonstrate how outer hair cells move to generate these emissions.

Hair Cells Internal Pressure

The cochlear outer hair cell (OHC) is a cylindrical cell with structural features suggestive of a hydraulic skeleton, i.e., an elastic shell with a positive internal pressure. One study characterizes the role of the OHC elevated cytoplasmic pressure in maintaining the cell shape. Intracellular pressure of OHCs from guinea pigs is estimated by measuring changes in cell morphology in response to increasing or decreasing osmolarity. Cells collapse when subjected to a continuous increase in osmolarity ooccurring at an average of 8 mosM above the standard medium, suggesting that normal cells have an effective intracellular pressure of 128 mmHg. Fewer cells collapse when exposed to slow rates of osmolarity increase than cells exposed to fast rates of osmolarity increase, although the final change in osmolarity in the perfusion chamber is similar. Furthermore, cells undergo a slow, spontaneous increase in volume on exposure to either no osmolarity change or slow rates of osmolarity increase, suggesting that the cell’s internal osmolarity increases in vitro. After volume reduction or elevation, cells do not return to their initial volume.

Electromotility

Brownell (1990) indicated that 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 (or generator) 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.  Dr. Brownell developed his theories and proved their validity working with hearing scientists in laboratories both in the US and abroad.  His greatest recognition undoubtedly comes from the large number of young hearing scientist and clinicians now examining hair cell function.  Work done in several laboratories, including his own, has now established hair cell motility as a key mechanism in active cochlear tuning and has tentatively identified the structural basis for motility. 

Hair Cell Rock and Roll

Since the amplitude, and hence the mechanical energy, of airborne sounds is tiny, the cochlea mechanically amplifies the incoming vibrations. The motors which supply this mechanical amplification are the outer hair cells. Like inner hair cells, they use stretch receptors associated with the stereocilia at their tips to sense vibrations and convert them to electrical currents. But only in outer hair cells are these currents used to control length changes which parallel, and reinforce, the incoming mechanical vibration. The video (Right), which was recorded in the laboratory of Prof. Jonathan Ashmore at University College London and first seen on the BBC in 1987.  It demonstrates what happens to an isolated guinea pig outer hair cell with a whole cell patch electrode attached. Through the pipette, an alternating current signal is injected, and the resulting motor response is observed under a microscope. The alternating current signal is also played to a loudspeaker, so we can hear the signal that the outer hair cell receives.  Click on the green Hair cell picture on the RIGHT and watch the Hair Cell Rock and Roll…..