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Hearing
The sense of hearing is based on the physics of sound and the physiology of the
external, middle, and inner ear, the nerves to the brain, and the brain parts involved
in processing acoustic information.
Sound Transmission in the Ear
The first step in hearing is the entrance of sound waves into the external auditory
canal. The shapes of the outer ear (the pinna, or auricle) and the external auditory
canal help to amplify and direct the sound. The sound waves reverberate from the
sides and end of the external auditory canal, filling it with the continuous vibrations of
pressure waves.
The tympanic membrane (eardrum) is stretched across the end of the external
auditory canal, and air molecules push against the membrane, causing it to vibrate at
the same frequency as the sound wave. Under higher pressure during a zone of
compression, the tympanic membrane bows inward. The distance the membrane
moves, although always very small, is a function of the force with which the air
molecules hit it and is related to the sound pressure and therefore its loudness. During
the subsequent zone of rarefaction, the membrane returns to its original position. The
exquisitely sensitive tympanic membrane responds to all the varying pressures of the
sound waves, vibrating slowly in response to low-frequency sounds and rapidly in
response to high-frequency ones.
The tympanic membrane separates the external auditory canal from the middle ear
cavity, an air-filled cavity in the temporal bone of the skull. The pressures in the
external auditory canal and middle ear cavity are normally equal to atmospheric
pressure. The middle ear cavity is exposed to atmospheric pressure through the
auditory (eustachian) tube, which connects the middle ear to the pharynx. The
slitlike ending of this tube in the pharynx is normally closed, but muscle movements
open the tube during yawning, swallowing, or sneezing, and the pressure in the
middle ear equilibrates with atmospheric pressure. A difference in pressure can be
produced with sudden changes in altitude (as in an ascending or descending elevator
or airplane), when the pressure outside the ear and in the ear canal changes while the
pressure in the middle ear remains constant because the auditory tube is closed. This
pressure difference can stretch the tympanic membrane and cause pain.
The second step in hearing is the transmission of sound energy from the tympanic
membrane through the middle-ear cavity to the inner ear. The inner ear, called the
cochlea, is a fluid-filled, spiral-shaped passage in the temporal bone. The temporal
bone also houses other passages, including the semicircular canals, which contain the
sensory organs for balance and movement. These passages are connected to the
cochlea but will be discussed later.
Because liquid is more difficult to move than air, the sound pressure transmitted to the
inner ear must be amplified. This is achieved by a movable chain of three small
bones, the malleus, incus, and stapes; these bones act as a piston and couple the
motions of the tympanic membrane to the oval window, a membrane covered
opening separating the middle and inner ear.
The total force of a sound wave applied to the tympanic membrane is transferred to
the oval window, but because the oval window is much smaller than the tympanic
membrane, the force per unit area (that is, the pressure) is increased 15 to 20 times.
Additional advantage is gained through the lever action of the middle-ear bones. The
amount of energy transmitted to the inner ear can be lessened by the contraction of
two small skeletal muscles in the middle ear that alter the tension of the tympanic
membrane and the position of the stapes in the oval window. These muscles help to
protect the delicate receptor apparatus of the inner ear from continuous intense sound
stimuli and improve hearing over certain frequency ranges. The entire system
described thus far has been concerned with the transmission of sound energy into the
cochlea, where the receptor cells are located. The cochlea is almost completely
divided lengthwise by a fluid-filled membranous tube, the cochlear duct, which
follows the cochlear spiral. On either side of the cochlear duct are fluid-filled
compartments: the scala vestibuli, which is on the side of the cochlear duct that ends
at the oval window; and the scala tympani, which is below the cochlear duct and
ends in a second membrane-covered opening to the middle ear, the round window.
The scala vestibule and scala tympani meet at the end of the cochlear duct at the
helicotrema.
Sound waves in the ear canal cause in-and-out movement of the tympanic membrane,
which moves the chain of middle-ear bones against the membrane covering the oval
window, causing it to bow into the scala vestibuli and back out (Figure 9–37),
creating waves of pressure there. The wall of the scala vestibule is largely bone, and
there are only two paths by which the pressure waves can be dissipated. One path is to
the helicotrema, where the waves pass around the end of the cochlear duct into the
scala tympani and back to the round-window membrane, which is then bowed out into
the middle ear cavity.
However, most of the pressure is transmitted from the scala vestibuli across the
cochlear duct. One side of the cochlear duct is formed by the basilar membrane
(Figure 9–38), upon which sits the organ of Corti, which contains the ear’s sensitive
receptor cells. Pressure differences across the cochlear duct cause vibration of the
basilar membrane.
The region of maximal displacement of the vibrating basilar membrane varies with
the frequency of the sound source. The properties of the membrane nearest the middle
ear are such that this region vibrates most easily—that is, undergoes the greatest
movement, in response to high-frequency (high-pitched) tones. As the frequency of
the sound is lowered, vibration waves travel out along the membrane for greater
distances. Progressively more distant regions of the basilar membrane vibrate
maximally in response to progressively lower tones.
Hair Cells of the Organ of Corti
The receptor cells of the organ of Corti, the hair cells, are mechanoreceptors that have
hairlike stereocilia protruding from one end. The hair cells transform the pressure
waves in the cochlea into receptor potentials. Movements of the basilar membrane
stimulate the hair cells because they are attached to the membrane.
The stereocilia are in contact with the overhanging tectorial membrane, which
projects inward from the side of the cochlea. As the basilar membrane is displaced by
pressure waves, the hair cells move in relation to the tectorial membrane, and,
consequently, the stereocilia are bent. Whenever the stereocilia bend, ion channels in
the plasma membrane of the hair cell open, and the resulting ion movements
depolarize the membrane and create a receptor potential.
Efferent nerve fibers from the brainstem regulatethe activity of certain of the hair
cells and dampen their response, which protects them. Despite this protective action,
the hair cells are easily damaged or even completely destroyed by exposure to highintensity noises such as amplified rock music concerts, engines of jet planes, and
revved-up motorcycles. Lesser noise levels also cause damage if exposure is chronic.
Hair cell depolarization leads to release of the neurotransmitter glutamate (the same
neurotransmitter released by photoreceptor cells), which binds to and activates
protein binding sites on the terminals of the 10 or so afferent neurons that synapse
upon the hair cell. This causes the generation of action potentials in the neurons, the
axons of which join to form the cochlear nerve (a component of cranial nerve VIII).
The greater the energy (loudness) of the sound wave, the greater the frequency of
action potentials generated in the afferent nerve fibers. Because of its position on the
basilar membrane, each hair cell and, therefore, the nerve fibers that synapse upon it
respond to a limited range of sound frequency and intensity, and they respondbest to a
single frequency
.
Neural Pathways in Hearing
Cochlear nerve fibers enter the brainstem and synapse with interneurons there, fibers
from both ears often converging on the same neuron. Many of these interneurons are
influenced by the different arrival times and intensities of the input from the two ears.
The different arrival times of low-frequency sounds and the difference in intensities of
high-frequency sounds are used to determine the direction of the sound source.
If, for example, a sound is louder in the right ear or arrives sooner at the right ear than
at the left, we assume that the sound source is on the right. The shape of the outer ear
(the pinna) and movements of the head are also important in localizing the source of a
sound. From the brainstem, the information is transmitted via a multineuron pathway
to the thalamus and on to the auditory cortex. The neurons responding to different
pitches (frequencies) are arranged along the auditory cortex in an orderly manner in
much the same way that signals from different
regions of the body are represented at different sites in the somatosensory cortex.
Different areas of the auditory system are further specialized, some neurons
responding best to complex sounds such as those used in verbal communication,
whereas others signal the location, movement, duration, or loudness of a sound.
Electronic devices can help compensate for damage to the intricate middle ear,
cochlea, or neural structures.
Hearing aids amplify incoming sounds, which then pass via the ear canal to the same
cochlear mechanisms used by normal sound. When substantial damage has occurred,
however, and hearing aids cannot correct the deafness, electronic devices known as
cochlear implants may restore functional hearing. In response to sound, cochlear
implants directly stimulate the cochlear nerve with tiny electric currents so that sound
signals are transmitted directly to the auditory pathways, bypassing the cochlea.
Vestibular System
Changes in the motion and position of the head are detected by hair cells in the
vestibular apparatus of the inner ear, a series of fluid-filled membranous tubes that
connect with each other and with the cochlear duct. The vestibular apparatus consists
of three membranous semicircular ducts and two saclike swellings, the utricle and
saccule, all of which lie in tunnels (canals) in the temporal bone on each side of the
head. The bony canals of the inner ear in which the vestibular apparatus and cochlea
are housed have such a complicated shape that they are sometimes called the
labyrinth. The canals that house the semicircular ducts are the semicircular canals
(a term often used to denote the semicircular ducts).
sThe Semicircular Canals The semicircular ducts detect angular acceleration
during rotation of the head along three perpendicular axes. The three axes of the
semicircular canals and the ducts within them are those activated while nodding the
head up and down as in signifying “yes,” shaking the head from side to side as in
signifying “no,” and tipping the head so the ear touches the shoulder Receptor cells
of the semicircular ducts like those of the organ of Corti, contain hairlike stereocilia.
These stereocilia are closely ensheathed by a gelatinous mass, the cupula, which
extends across the lumen of each semicircular duct at the ampulla, a slight bulge in
the wall of each duct.
Whenever the head is moved, the bony semicircular canal, its enclosed duct, and the
attached bodies of the hair cells all move with it. The fluid filling the duct, however,
is not attached to the skull, and because of inertia, tends to retain its original position
(that is, to be “left behind”).
Thus, the moving ampulla is pushed against the stationary fluid, which causes
bending of the stereocilia and alteration in the rate of release of a chemical transmitter
from the hair cells. This transmitter activates the nerve terminals synapsing with the
hair cells.
The speed and magnitude of rotational head movements determine the direction in
which the stereocilia are bent and the hair cells stimulated. Neurotransmitter
is released from the hair cells at rest, and the release changes from this resting rate
according to the direction in which the hairs are bent. Each hair cell receptor has one
direction of maximum neurotransmitter release, and when its stereocilia are bent in
this direction, the receptor cell depolarizes. When the stereocilia are bent in the
opposite direction, the cell hyperpolarizes. The frequency of action potentials in the
afferent nerve fibers that synapse with the hair cells is related to both the amount of
force bending the stereocilia on the receptor cells and to the direction in which this
force is applied.
At a constant velocity, the duct fluid begins to move at the same rate as the rest of the
head, and the stereocilia slowly return to their resting position. For this reason, the
hair cells are stimulated only during changes in the rate of rotation (that is, during
acceleration or deceleration) of the head.
The Utricle and Saccule
The utricle and saccule provide information about linear— up and down, back and
forth—acceleration and changes in head position relative to the forces of gravity.
Here, too, the receptor cells are mechanoreceptors sensitive to the displacement of
projecting hairs. The patch of hair cells in the utricle is nearly horizontal in a standing
person, and that in the saccule is vertical. The stereocilia projecting from the hair cells
are covered by a gelatinous substance in which tiny stones, or otoliths, are embedded;
the otoliths, which are calcium carbonate crystals, make the gelatinous substance
heavier than the surrounding fluid. In response to a change in position, the gelatinous
otolithic material moves according to the forces of gravity and pulls against the hair
cells so that the stereocilia on the hair cells are bent and the receptor cells stimulated.
Vestibular Information and Dysfunction
Information about hair cell stimulation is relayed from the vestibular apparatus to the
brainstem via the vestibular branch of cranial nerve VIII (the same cranial nerve that
carries acoustic information). It is transmitted via a multineuronal pathway to a
system of vestibular centers in the parietal lobe. Vestibular information is integrated
with information from the joints, tendons, and skin, leading to the sense of posture
and movement. Vestibular information is used in three ways. One is to control the eye
muscles so that, in spite of changes in head position, the eyes can remain fixed on the
samepoint.
Nystagmus is a large, jerky, back-and-forth movement of the eyes that can occur in
response to unusual vestibular input in normal people but can also be a pathological
sign. The second use of vestibular information is in reflex mechanisms for
maintaining upright posture. The vestibular apparatus plays a role in the support of the
head during movement, orientation of the head in space, and reflexes accompanying
locomotion. Very few postural reflexes, however, depend exclusively on input from
the vestibular system despite the fact that the vestibular organs are sometimes called
the sense organs of balance. The third use of vestibular information is in providing
conscious awareness of the position and acceleration of the body, perception of the
space surrounding the body, and memory of spatial information. Unexpected inputs
from the vestibular system and other sensory systems such as those caused by a
stroke, irritation of the labyrinths by infection, or even loose particles of calcium
carbonate in the semicircular ducts can induce vertigo, defined as an illusion of
movement— usually spinning—that is often accompanied by feelings of nausea and
lightheadedness. This can also occur when there is a mismatch in information
from the various sensory systems as, for example, when one is in a high place looking
down to the ground: The visual input indicates that you are floating in space while the
vestibular system signals that you are not moving at all. Motion sickness also
involves the vestibular system, occurring when unfamiliar patterns of linear and
rotational acceleration are experienced and adaptation to them has not occurred.
Ménière’s disease involves the vestibular system and is associated with episodes of
abrupt and often severe dizziness, ringing in the ears, and bouts of hearing loss. It is
due to an increased fluid pressure in the membranous duct system of the inner ear.
The dizziness occurs because the inputs from the two ears are not balanced, either
because only one ear is affected or because the two are affected to different degrees.
Chemical Senses
Receptors sensitive to specific chemicals are chemoreceptors. Some of these respond
to chemical changes in the internal environment, two examples being the oxygen and
hydrogen-ion receptors in certain large blood vessels. Others respond to external
chemical changes, and in this category are the receptors for taste and smell, which
affect a person’s appetite, saliva flow, gastric secretions, and avoidance of harmful
substances.
Taste
The specialized sense organs for taste are the 10,000 or so taste buds that are found
primarily on the tongue. The receptor cells are arranged in the taste buds like the
segments of an orange. A long narrow process on the upper surface of each receptor
cell extends into a small pore at the surface of the taste bud, where the process is
bathed by the fluids of the mouth.
Many chemicals can generate the sensation of taste, but taste sensations (modalities)
are traditionally divided into four basic groups: sweet, sour, salty, and bitter, each
group having a distinct transductional system. For example, salt taste begins with
sodium entry into the cell through plasma-membrane ion channels, which depolarizes
the plasma membrane; depolarization causes neurotransmitter release from the
receptor cell at synapses with afferent nerve fibers. In contrast, molecules such as
carbohydrates interact with plasmamembrane receptors that regulate secondmessenger cascades. It is likely that different mechanisms occur in separate cell types.
Although more than one afferent fiber synapses with each receptor cell, the taste
system is organized into independent coded pathways into the central nervous system.
Single receptor cells, however, respond in varying degrees to substances that fall into
more than one taste category and awareness of the specific taste of a substance
depends also upon the pattern of firing in a group of neurons. For example, sensations
of pain (“hot” spices), texture, and temperature contribute to taste. The pathways for
taste in the central nervous system project to the parietal cortex, near the “mouth”
region of the somatosensory cortex.
Smell
Eighty percent of the flavor of food is actually contributed by the sense of smell, or
olfaction, as is attested by the common experience that food lacks taste when one has
a head cold. The odor of a substance is directly related to its chemical structure. Since
we are able to recognize and identify hundreds of different odors with a great deal of
accuracy, neural circuits that deal with olfaction must encode information about
different chemical structures, store (learn) the different code patterns that represent
the different structures, and at a later time recognize a particular neural code to
identify the odor. The olfactory receptor cells, the first cells in the pathways that give
rise to the sense of smell, lie in a small patch of membrane, the olfactory epithelium,
in the upper part of the nasal cavity. These cells are specialized afferent neurons that
have a single enlarged dendrite that extends to the surface of the
epithelium. Several long nonmotile cilia extend out from the tip of the dendrite and lie
along the surface of the olfactory epithelium where they are bathed in mucus.
The cilia contain the receptor proteins (binding sites) for olfactory stimuli. The axons
of the neurons form the olfactory nerve, which is cranial nerve I.
For an odorous substance (that is, an odorant) to be detected, molecules of the
substance must first diffuse into the air and pass into the nose to the region of the
olfactory epithelium. Once there, they dissolve in the mucus that covers the
epithelium and then bind to specific odorant receptors on the cilia. Proteins in the
mucus may interact with the odorant molecules, transport them to the receptors, and
facilitate their binding to the receptors. Although there are many thousands of
olfactory receptor cells, each contains one, or at most a few, of the 1000 or so
different plasma-membrane odorant receptor types, each of which responds only to a
specific chemically related group of odorant molecules. Each odorant has
characteristic chemical groups that distinguish it from other odorants, and each of
these groups activates a different plasma-membrane odorant receptor type. Thus, the
identity of a particular odorant is determined by the activation of a precise
combination of plasma-membrane receptors, each of which is contained in a distinct
group of olfactory receptor cells. The axons of the olfactory receptor cells synapse
in the brain structures known as olfactory bulbs, which lie on the undersurface of the
frontal lobes. Axons from olfactory receptor cells sharing a common receptor
specificity synapse together on certain olfactory-bulb neurons, thereby maintaining
the specificity of the original stimulus. In other words, specific odorant receptor cells
activate only certain olfactory-bulb neurons, thereby allowing the brain to
determine which receptors have been stimulated. The codes used to transmit olfactory
information probably use both spatial (which neurons are firing?) and temporal (what
is the timing of the action-potential responses?) components. Information is passed
from the olfactory bulbs to olfactory cortex, which is in the limbic system (see Figure
8–42), a part of the brain intimately associated with emotional, food-getting, and
sexual behavior. There, different odors elicit different patterns of electrical activity
in a variety of cortical areas, allowing humans to discriminate between some 10,000
different odorants even though they have only 1000 different olfactory receptor types.
Olfactory discrimination varies with attentiveness: hunger—sensitivity is greater in
hungry subjects; gender— women in general have keener olfactory sensitivities
than men; smoking—decreased sensitivity has been repeatedly associated with
smoking; age—the ability to identify odors decreases with age, and a large percentage
of elderly persons cannot detect odors at all; and state of the olfactory mucosa—as we
have mentioned, the sense of smell decreases when the mucosa is congested, as in a
head cold.