How do we hear? According to researchers from the Stanford University School of Medicine, the old-school scientific model explaining that process has gotten it all wrong. Used for the past three decades, the former theory illuminated a component of hearing called "adaptation" — the reason why humans can perceive everything from a mouse squeak to a jet engine with high acuity yet without pain or damage to the ear. Now, a team of Stanford researchers claim that a necessary part of the adaptation process, mechanotransduction — the conversion of mechanical signals into chemical signals — does not work the way scientists originally theorized.

"I would argue that adaptation is probably the most important step in the hearing process, and this study shows we have no idea how it works," Anthony Ricci, PhD, professor of Otolaryngology and senior author of the study, stated in a press release.

Clarification Necessary

“The hearing field has such precise models — models that everyone uses,” Ulrich Mueller, PhD, professor of molecular and cellular neuroscience at the Scripps Research Institute, said in the statement. “When one of the models tumbles, it's monumental.”

What is known is this: Specialized cells that are located deep inside the ear detect vibrations caused by air pressure differences. These sensory cells, known as hair cells, convert the vibrations into electrochemical signals that the brain interprets as sound, with adaptation being the process that enables these cells to regulate the decibel range over which they operate. This key process, something like a volume switch on a speaker, protects the ear by adjusting our sensitivity to the noise level.

Traditionally, scientists explained how this "adaptation" works by saying it is regulated by at least two complex cellular mechanisms both of which require calcium entry through a specific ion channel in the hair cells. One problem with this explanation — and the weakness exploited by the Stanford scientists — is that all the supporting research was conducted on frogs and turtles, not mammals.

Reptiles and Amphibians Need Not Apply

Experimenting primarily on rats, the Stanford scientists used mechanical stimulation to elicit responses from the hair cells while they tracked calcium signals, using high-speed, high-resolution imaging, before they had time to diffuse. After manipulating the intracellular calcium in various ways, the scientists discovered that calcium was not necessary for adaptation to occur. Effectively, then, they overturned a working theory for the past three decades and paved the way for new hypotheses of mechanotransduction and adaptation.

"This somewhat heretical finding suggests that at least some of the underlying molecular mechanisms for adaptation must be different in mammalian cochlear hair cells as compared to that of frog or turtle hair cells, where adaptation was first described," Ricci said in the press release. “Hearing damage … can target this particular molecular process. It's by understanding just how the inner machinery of the ear works that scientists hope to eventually find ways to fix the parts that break."

Each of us is born with 30,000 hair cells in each ear, distributed throughout the cochlea (a spiral cavity in the ear) and vestibule (a portion of the inner ear). Hearing loss occurs when too many of these cells are lost or damaged, which can be caused by multiple reasons, with aging and noise pollution (can you hear me? You, with the ear buds.) among them. Unlike other species, humans and other mammals do not spontaneously regenerate hair cells. Health experts estimate that one in three adults over the age of 65 has developed at least some degree of hearing disability due to destruction of this finite number of hair cells.

Source: Peng AW, Effertz T, Ricci AJ. Adaptation of Mammalian Auditory Hair Cell Mechanotransduction Is Independent of Calcium Entry. Neuron. 2013.