Overall, how we hear is still a complicated process with many unanswered questions. However, for low pitch sounds such as a tuba or trombone, those waves travel deeper into the cochlea before being translated (15, 16). In the case of high pitch sounds such as a flute or piccolo, waves travel a very short distance in the cochlea before being translated into what we hear. As for pitch, different frequency waves are able to travel different distances within the cochlea.
Hear ye hear ye tv#
This process, known as adaptation, can explain why putting the TV on volume 8 is sufficient in the quiet of the night, but way too quiet of a volume when watching in the loud and busy midday (Figure 3). Interestingly, the sensitivity of these channels can also be changed to protect the ear from sounds that are too loud. This potential causes an electrical signal to be sent from the auditory nerve to the brain, thus resulting in sound (14). As the channels open, K + ions flood into the hair cells and cause a change in membrane potential. As the stereocilia tilt, membrane tension changes and Myo7A is able to walk in a tip-ward direction, opening the channels. This movement facilitates the opening of the mechanoelectrical transduction (MET) channels, as the channels are located at the stereocilia tips and are connected to the tip link region of adjacent stereocilia via the same protein linkers as Myo7A (13). Photo Credit: Jeroom, adapted by Joe CiriloĪs the sound wave is conducted through the endolymph, the vibration of the waves causes the stereocilia to move. Overall, these molecular motors work hand in hand to maintain stereocilia structure and morphology.įigure 3: Meme describing how MET channels adjust to sound in different environments. Complete loss of Myo3A has been shown to cause extremely long stereocilia, while mutations have been shown to cause both unregulated protrusion size and dynamics(11, 12). Myo3A also tip localizes, however its overall function is still unknown. Myo15A has been previously shown to help initiate elongation of stereocilia, with mutations leading to unregulated lengths and hearing loss (8).
Lastly, at the stereocilia tip are Myosins 3A and 15A. Myo1C also can be found localized to this region, though its overall function is still widely unknown (10). Mutations in Myo7A have been demonstrated to be associated with dysregulated morphology of stereocilia, resulting in hearing loss (7). Within this region, Myo7A interacts with a complex of proteins to connect the two protrusions together(9). Further up the stereocilia, found at the region in which the stereocilia is connected to its smaller neighbor, is the tip-link region. The anklet, found at the base of the stereocilia, contains Myo6 which links the membrane of the stereocilia to its actin core(5). These myosins generally localize to one of three different areas of the stereocilia: the tip, the tip-link, or the anklet (4-8).
Charged with maintaining the structure of stereocilia are numerous classes of the molecular motor myosin, including myosin 1C (Myo1C), myosin 3A (Myo3A), myosin 6 (Myo6), myosin 7A (Myo7A), and myosin 15A Myo15A (Figure 2). This structure is imperative to the hearing process throughout an organism’s life, with many studies detailing how altered morphology leads to hearing loss. During development, stereocilia form into a staircase-like structure of varying row heights (Figure 1) (3). Stereocilia are hair-like protrusions formed of a tightly bundled parallel actin core, numerous membrane linkers, and important ion channels that help conduct the hearing process. Figure 2: Depiction of myosin localization throughout the stereocilia, from Peng et al.