For the past three decades, scientists have widely believed that the way humans and other animals adapt to sounds at different volumes was a two step-process, both relying on calcium to function. Now hear this: A new study from Stanford otolaryngologists suggests this isn't the case - and the findings could fundamentally change the way doctors treat hearing loss.
As Tracie White describes today in our release:
Deep inside the ear, specialized cells called hair cells detect vibrations caused by air pressure differences and convert them into electrochemical signals that the brain interprets as sound. Adaptation is the part of this process that enables these sensory hair cells to regulate the decibel range over which they operate. The process helps protect the ear against sounds that are too loud by adjusting the ears’ sensitivity to match the noise level of the environment.
The traditional explanation for how adaptation works, based on earlier research on frogs and turtles, is that it is controlled by at least two complex cellular mechanisms both requiring calcium entry through a specific, mechanically sensitive ion channel in auditory hair cells. The new study, however, finds that calcium is not required for adaptation in mammalian auditory hair cells and posits that one of the two previously described mechanisms is absent in auditory cochlear hair cells.
Experimenting mostly on rats, the Stanford scientists used ultrafast mechanical stimulation to elicit responses from hair cells as well as high-speed, high-resolution imaging to track calcium signals quickly before they had time to diffuse. After manipulating intracellular calcium in various ways, the scientists were surprised to find that calcium was not necessary for adaptation to occur, thus challenging the 30-year-old hypothesis and opening the door to new models of mechanotransduction (the conversion of mechanical signals into electrical signals) and adaptation.
Anthony Ricci, PhD, senior author of the study, explained, “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. So when a key piece of the puzzle is shown to be wrong, it’s of extreme importance to scientists working to cure hearing loss.”
The study was published today in Neuron. Postdoctoral scholar Anthony Peng, PhD, is the lead author.
Previously: Stanford researchers gain new insights into how auditory neurons develop in animal study, Stanford chair of otolaryngology discusses future regenerative therapies for hearing loss and Stanford engineer studies bones that aid hearing
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