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Basilar Membrane And Vestibular Membrane
3,000 Hz j\_

Medium pitch: Pressure waves travel only part of the way down the upper canal before flexing the basilar membrane and activating mid-frequency sensors.

Medium pitch: Pressure waves travel only part of the way down the upper canal before flexing the basilar membrane and activating mid-frequency sensors.

22,000 Hz

High pitch: Pressure waves travel a short distance before flexing the basilar membrane and activating high-frequency sensors.

22,000 Hz

High pitch: Pressure waves travel a short distance before flexing the basilar membrane and activating high-frequency sensors.

If the oval window vibrates in and out rapidly, the waves of fluid pressure do not have enough time to travel all the way to the end of the upper canal and back through the lower canal. Instead, they take a shortcut by crossing the basilar membrane, causing it to flex. The more rapid the vibration, the closer to the oval and round windows the pressure wave will flex the basilar membrane. Thus, different pitches of sound flex the basilar membrane at different locations and activate different sets of hair cells.

The ability of the basilar membrane to respond to vibrations of different frequencies is enhanced by its structure. Near the oval and round windows, at the proximal end, the basilar membrane is narrow and stiff, but it gradually becomes wider and more flexible toward the opposite (distal) end. So it is easier for the proximal basilar membrane to resonate with high frequencies and for the distal basilar membrane to resonate with lower frequencies. A complex sound made up of many frequencies distorts the basilar membrane at many places simultaneously and activates a unique subset of hair cells. Action potentials stimulated by the mechanoreceptors at different positions along the organ of Corti travel to the brain stem along the auditory nerve.

Deafness, the loss of the sense of hearing, has two general causes. Conduction deafness is caused by the loss of function of the tympanic membrane and the ossicles of the middle ear. Repeated infections of the middle ear can cause scarring of the tympanic membrane and stiffening of the connections between the ossicles. The consequence is less efficient conduction of sound waves from the tympanic membrane to the oval window. With increasing age, the ossicles progressively stiffen, resulting in a gradual loss of the ability to hear high-frequency sounds. Nerve deafness is caused by damage to the inner ear or the auditory pathways. A common cause of nerve deafness is damage to the hair cells of the delicate organ of Corti by exposure to loud sounds such as jet engines, pneumatic drills, or highly amplified music. This damage is cumulative and permanent.

mation. A rhodopsin molecule consists of a protein, opsin (which alone is not photosensitive), and a light-absorbing prosthetic group, 11-cis-retinal. The light-absorbing group is cradled in the center of the opsin and is bound covalently to it. The entire rhodopsin molecule sits within the plasma membrane of a photoreceptor cell (Figure 45.12).

When the 11-cis-retinal absorbs a photon of light energy, it changes into a different isomer of retinal, called all-trans-retinal. This change puts a strain on the bonds between retinal and opsin, changing the conformation of opsin. This change signals the detection of light. In vertebrate eyes, the retinal and the opsin eventually separate from each other—a process called bleaching, which causes the molecule to lose its photo-sensitivity. A series of enzymatic reactions is then required to return the all-trans retinal to the 11-cis isomer, which then recombines with opsin so that it once again becomes the photosensitive pigment rhodopsin.

How does the conformational change of rhodopsin transduce light into a cellular response? After retinal is converted from the 11-cis into the all-irans form, its interactions with

Opsin

Plasma membrane

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