The Ear: Hearing
given bud, tight junctions link the apical ends of adjacent cells
together, limiting movement of molecules between the cells.
The apical membrane of a taste cell is modified into microvilli
to increase the amount of surface area in contact with the en­
vironment (Fig. 10-16c).
For a substance (tastant) to be tasted, it must first dissolve
in the saliva and mucus of the mouth. Dissolved taste ligands
then interact with an apical membrane protein (receptor or
channel) on a taste cell (Fig. 10-16c). Although the details of
signal transduction for the five taste sensations are still contro­
versial, interaction of a taste ligand with a membrane protein
initiates a signal transduction cascade that ends with a series of
action potentials in the primary sensory neuron.
The mechanisms of taste transduction are a good example
of how our models of physiological function must periodically
be revised as new research data are published. For many years
the widely held view of taste transduction was that an individ­
ual taste cell could sense more than one taste, with cells differ­
ing in their sensitivities. However, gustation research using mo­
lecular biology techniques and knockout mice [ ~ jJ 292J
currently indicates that each taste cell is sensitive to only one
taste.
In the old model , all taste cells formed synapses with pri­
mary sensory neurons called gustatory neurons. Now it has
been shown that there are two different types of taste cells,
and that only the taste cells for salty and sour tastes (type III
or presynaptic cells) synapse with gustatory neurons. The
presynaptic taste cells release the neurotransmitter serotonin
byexocytosis.
The taste cells for sweet, bitter, and umami sensations
(type II or receptor cells) do not form traditional synapses.
Instead they release ATP through gap junction-like channels,
and the ATP acts both on sensory neurons and on neighboring
presynaptic cells. This communication between neighboring
taste cells creates complex interactions.
Taste Transduction Uses Receptors
and Channels
The details of taste cell signal transduction, once thought to be
relatively straightforward, are also more complex than scien­
tists initially thought (Fig. 10-17 e ). The type II taste cells for
bitter, sweet, and umami tastes express different G protein­
coupled receptors, including about 30 variants of bitter recep­
tors. In type II taste cells, the receptor proteins are associated
with a special G protein called gustducin.
Gustducin appears to activate multiple signal transduc­
tion pathways. Some pathways release Ca 2 + from intracellular
stores, while others open cation channels and allow Ca 2 + to
enter the cell. Calcium signals then initiate ATP release from
the type II taste cells.
In contrast, salty and sour transduction mechanisms
both appear to be mediated by ion channels rather than by
353
G protein-coupled receptors. In the current model for salty
tastes, Na + enters the presynaptic cell through an apical
channel and depolarizes the taste cell, resulting in exocytosis
of the neurotransmitter serotonin. Serotonin in turn excites
the primary gustatory neuron.
Transduction mechanisms for sour tastes are more contro­
versial, complicated by the fact that increasing H+, the sour
taste signal, also changes pH. There is evidence that H+ acts on
ion channels from both extracellular and intracellular sides of
the membrane, and the transduction mechanisms remain un­
certain. Ultimately, H+-mediated depolarization of the presyn­
aptic cell results in serotonin release, as described for salt taste
above.
Neurotransmitters (ATP and serotonin) from taste cells ac­
tivate primary gustatory neurons whose axons run through cra­
nial nerves VII, IX, and X to the medulla, where they synapse.
Sensory information then passes through the thalamus to the
gustatory cortex (see Fig. 10-4). Central processing of sensory
information compares the input from multiple taste cells and
interprets the taste sensation based on which populations of
neurons are responding most strongly. Signals from the sensory
neurons also initiate behavioral responses, such as feeding, and
feedforward responses [ ~ fl. 2ll-l-J that activate the digestive
system.
An interesting psychological aspect of taste is the phe­
nomenon named specific hunger. Humans and other animals
that are lacking a particular nutrient may develop a craving for
that substance. Salt appetite, representing a lack of Na+ in the
body, has been recognized for years. Hunters have used their
knowledge of this specific hunger to stake out salt licks because
they know that animals will seek them out. Salt appetite is di­
rectly related to Na+ concentration in the body and cannot be
assuaged by ingestion of other cations, such as Ca 2 + or K+.
Other appetites, such as cravings for chocolate, are more diffi­
cult to relate to specific nutrient needs and probably reflect
complex mixtures of physical, psychological, environmental,
and cultural influences.
CONCEPT
CHECK
14. With what essential nutrient is the umami taste sensation as­
sociated?
1S. Map or diagram the neural pathway from a presynaptic taste
cell to the gustatory cortex.
Answ ers p. 383
THE EAR: HEARING
The ear is a sense organ that is specialized for two distinct func­
tions: hearing and equilibrium. It can be divided into external,
middle, and inner sections, with the neurological elements
housed in and protected by structures in the inner ear. The
vestibular complex of the inner ear is the primary sensor for
equilibrium. The remainder of the ear is used for hearing.
10
354
Chapter 10 Sensory Physiology
0Gustducin
0
1
Sour
Sweet, umami ,
or bitter ligand
@
/0
GPCR
Ligands activate the taste cell.
Various intracellular pathways
are activated.
~) Ca2• signal in the cytoplasm
triggers exocytosis or ATP
formation .
o :•""":-­- - ­ Primary gustatory
neurons
Serotonin
Neurotransmitter or ATP is
released.
--~,.,
«) Primary sensory neuron fires
and action potentials are
sent to the brain.
e
FIGURE 10-17
Summary of taste transduction. Each taste cell senses only
one type of ligand. Receptor cells with G protein-coupled membrane receptors bind
either bitter, sweet, or umami ligands and release ATP as a signal molecule. Sodium ion
for salt taste enters presynaptic cel ls through ion channels and triggers exocytosis of
serotonin. It is unclear whether H+ for sour taste acts intracellularly or extracellularly.
The external ear consists of the outer ear, or pinna, and the
ear canal (Fig. 10-18 e ). The pinna is another exampJe of an
important accessory structure to a sensory system, and it vari es
in shape and location from species to species, depending on
the animals' survival needs . The ear canal is sealed at its inter­
nal end by a thin membranous sheet of tissue called the
tympanic membrane, or eardrum.
The tympanic membrane separates the external ear from
the middle ear, an air-filled cavity that connects with the phar­
ynx through the eustachian tube . The eustachian tube is nor­
mally collapsed, sealing off the middle ear, but it opens tran­
siently to allow middle ear pressure to eqUilibrate with
atmospheric pressure during chewing, swallOwing, and yawn­
ing. Colds or other infections that cause swelling can block the
eustachian tube and result in fluid buildup in the middle ear. If
bacteria are trapped in the middle ear fluid , the ear infection
known as otitis m edia [oto-, ear + -itis, inflammation + media,
middle] results.
Three small bones of the middle ear conduct sound from
the external environment to the inner ear: the malleus [ham­
mer], the incus [anvil], and the stapes [stirrup]. The three
bones are connected to one another with the biological equiv­
alent of hinges. One end of the malleus is attached to the tym­
panic membrane, and the stirrup end of the stapes is attached
to a thin membrane that separates the middle ear from the
inner ear.
The Ear: Hearing
EME RGING CONCEPTS CHANGING TASTE
Sweet receptors respond to sugars, and umami
receptors respond to glutamate, covering two of the
three major groups of nutritious biomolecules. But
what about fats? For years physiologists thought it
was fat's texture that made it appealing, but now
it appears that the tongue may have receptors for
long-chain fatty acids, such as oleic acid [ ~r lfl ).
Research in rodents has identified a membr·a ne re­
ceptor called CD36 that lines taste pores and binds
fats. Activation of the receptor helps trigger the
feedforward digestive reflexes that prepare the
digestive system for a meal. Cur-rently evidence is
lacking for a similar receptor in humans, but "fatty"
may turn out to be a sixth taste sensation.
And what would you say to the idea of taste
buds in your gut? Scientists have known for years
that the stomach and intestines have the ability to
sense the composition of a meal and secrete appro­
priate hormones and enzymes. Now it appears that
gut chemoreception is being mediated by the same
receptors and signal transduction mechanisms that
occur in taste buds on the tongue . Studies have
found the T1 R receptor proteins for sweet and
umami tastes as well as the G protein gustducin in
various cells in rodent and human intestines.
The inner ear consists of two major sensory structures. The
vestibular apparatus with its semicircular canals is the sensory
transducer for our sense of equilibrium, described in the follow­
ing section. The cochlea of the inner ear contains sensory re­
ceptors for hearing. On external view the cochlea is a m embra­
nous tube that lies coiled like a snail shell within a bony cavity.
Two membranous disks, the oval window (to which the stapes
is attached) and the round window, separate the liquid-filled
cochlea from the air-filled middle ear. Bran ches of cranial nerve
VIII, the vestibulococl1lear nerve, lead from the inner ear to th e
brain.
Hearing Is Our Perception of Sound
Hearing is our perception of the energy carried by sound WaI'es,
which are pressure waves with alternating peaks of compressed
air and valleys in which the air molecules are farth er apart
(Fig. 10-19a e ). The classic question about hearing is, "If a tree
falls in the forest with no one to hear, does it make a noise?"
The physiological answer is no. The falling tree emits sound
355
waves, but there is no noise unless someone or something is
present to process and perceive the wave energy as sound.
Sound is the brain's interpretation of the frequenc y, ampli­
tude, and duration of sound waves that reach our ears . Our
brains translate frequency of sound waves (the number of
wave peaks that pass a given point each second) into the pitch
of a sound. Low-frequency waves are perceived as low-pitched
sounds, such as th e rumble of distant thunder. High-frequency
waves create high-pitched sounds, such as the screech of finger­
nails on a bl ackboard.
Sound wave frequency (Fig. 10-19b) is measured in waves
per second, or hertz (Hz). The average human ear can hear
sounds over the frequency range of 20-20,000 Hz, with the
most acute hearing between 1000-3000 Hz. Our hearing is not
as acute as that of many other animals, just as our sense of
smell is less acute. Bats listen for ultra-high-frequency sound
waves (in the kilohertz range) that bounce off objects in the
dark. Elephants and some birds can hear sounds in the infra­
sound (very low frequenc y) range .
Loudness is our interpretation of sound intensity and is
influenced by the sensitivity of an individual's ear. The inten­
sity of a sound wave is a function of the wave amplitude
(Fig . 1O-19b). Intensity is measured on a logarithmic scale in
units called decibels (dB). Each 10-dB increase represents a lO-fold
increase in intensity.
Normal conversation has a typical noise level of about 60 dB.
Sounds of 80 dB or more can damage the sensitive hearing re­
ceptors of the ear, resulting in hearing loss. A typical heavy
metal rock concert has noise levels around 120 dB, an intensity
that puts listeners in immediate danger of damage to their
hearing. The amount of damage depends on the duration and
frequency of the noise as well as its intensity.
CONCEPT
16.
What is a kilohertz?
CHECK
Answers p. 383
Sound Transduction Is a Multistep Process
Hearing is a complex sense that involves multiple transductions .
Energy from sound waves in the air becomes CD mechanical
vibrations, then ® fluid waves in the cochlea. The fluid waves
open ion channels in l1air cells, the sensory receptors for hearing.
Ion flow into hair cells creates @ electrical signals that release (3)
neurotransmitter (chemical signal), which in turn triggers ® ac­
tion potentials in the primary auditory neurons.
These transduction steps are shown in Figure 10-20 • .
Sound waves striking the outer ear are directed down the ear
canal until they hit the tympaniC membrane and cause it to vi­
brate (first transduction). The tympaniC membrane vibrations
are transferred to the malleus, the incus, and the stapes, in that
order. The arrangement of the three connected middle ear
o
356
Chapter 10 Sensory Physiology
THE EAR
EXTERNAL EAR
MIDDLE EAR
INNER EAR
\
~--------------~~~ \,\~--~----------------------------------------~~!
\
The pinna
directs sound
waves into
the ear
,
The oval window and the round window separate the fluid-filled inner ear from the air-filled middle ear. \
\
\
\
\
\
\
Malleus
Semicircular
canals
\
\
\
Oval window
Nerves \
\
Stapes '.
\
Tympanic
membrane
vein
•
Eustachian tube FIGURE 10-18
bones creates a "lever" th at multiplies the force of the vibration
(amplification ) so that very little sound energy is lost due to fric­
tion. If noise levels are so high that there is danger of damage
to the inner ear, small muscles in the middle ear can pull on
the bones to decrease their movement and thereby dampen
sound transmission to some degree .
As the stapes vibrates, it pulls and pushes on the thin tis­
sue of the oval window, to which it is attached. Vibrations at
the oval window create waves in the fluid-filled channels of the
cochlea (second transduction). As waves move through the
cochlea, they push on the flexible membranes of the cochlear
duct and bend sensory hair cells inside the duct. The wave en­
ergy dissipates back into the air of the middle ear at the round
window.
Movement of the cochlear duct opens or closes ion chan­
nels on hair cell membranes, creating electrical signals (third
transduction). These electrical signals alter neurotransmitter re­
lease (fourth transduction). Neurotransmitter binding to the
primary auditory neurons initiates action potentials (fifth
transduction) that send coded information about sound
through the cochlear branch of the vestibulocochlear nerve (cranial
nerve VlII) and the brain.
The Cochlea Is Filled with Fluid
The transduction of wave energy into action potentials takes
place in the cochlea of the inner ear. Uncoiled, the cochlea can
be seen to be composed of three parallel, fluid-filled channels:
The Ear: Hearing
RUNNING
357
PROBLEM
Anant reports to the otolaryngologist that he never knows when
his attacks of dizziness will strike and that they last from 10 min­
utes to an hour. They often cause him to vomit. He also reports
that he has a persistent low buzzing sound in one ear and that
he does not seem to hear low tones as well as he could before the
attacks started. The buzzing sound (tinnitus) often gets worse
during his dizzy attacks.
Tuning fork
(a) Sound waves alternate peaks of compressed air and valleys where
the air is less compressed.
(1)
Question 2:
Subjective tinnitus occurs when an abnormality somewhere
along the anatomical pathway for hearing causes the brain to
perceive a sound that does not exist outside the auditory sys­
tem. Starting from the ear canal, name the auditory struc­
tures in which problems may arise.
/ 1 Wavelength
1----41
339
Intensity
(dB)
e
-jAmPlitude
(dB)
o
Time (sec)
0.25
(2)
I",e"(~i~ ~ VVnVnVnVnVnVffvfivfi1r~~rli,"de
n
n
o
Time (sec)
0.25
•
(b) Sound waves are distinguished by their amplitude, measured in
decibels (dB), and frequency, measured in hertz (Hz).
FIGURE
QUESTIONS
• What are the frequencies of the
sound waves in graphs (1) and (2)
in Hz (waves/second)?
• Which set of sound waves would be
interpreted as having lower pitch?
• FIGURE 10-19
Sound waves
(1) the vestibular duct, or scala vestibuli [scala, stairway;
vestibulum, entrance]; (2) the central cochlear duct, or scala
media [media, middle] ; and (3) the tympanic duct, or scala tym­
pani [tympal1ol1 , drum] (Fig. 10-21 e ). The vestibular and tym­
panic ducts are continuous with each other, and they connect
at the tip of the cochlea through a small opening known as the
helicotrema [helix, a spiral + tJ'ema, hole]. The cochlear duct is
a dead-end tube but it connects to the vestibular apparatus
through a small opening.
The fluid in the vestibular and tympaniC ducts is similar in
ion composition to plasma and is known as perilymph. The
cochlear duct is filled with endolymph secreted by epithelial
cells in the duct. Endolymph is unusual because it is more like
intracellular fluid than extracellular fluid in composition, with
high concentrations of K+ and low concentrations of Na +.
The cochlear duct contains the organ of Corti, composed
of hair cell receptors and support cells. The organ of Corti sits
on the basilar membrane and is partially covered by the
tectorial membrane [tectorium, a cover], both flexible tissues
that move in response to fluid waves passing through the
vestibular duct (Fig. 10-21). As the waves travel through the
cochlea, they displace basilar and tectorial membranes, creat­
ing up-and-down oscillations that bend the hair cells.
Hair cells, like taste cells, are non-neural receptor cells .
The apical surface of each hair cell is modified into 50-100 stiff­
ened cilia known as stereocilia, arranged in ascending height
(Fig. 10-22a e ). The longest cilium of each hair cell, called a
kinocilium [kinein, to move] is embedded in the overlying tec­
torial membrane . If the tectorial membrane moves, the embed­
ded kinocilia do also. This movement is transmitted to the
stereocilia of the hair cell.
When hair cells move in response to sound waves, their
stereocilia flex, first one way, then the other. The stereocilia are
attached to each other by protein bridges called tip links . The
tip links act like little springs and are connected to gates that
o
358
Chapter 10 Sensory Physiology
Sound waves strike
the tympanic
membrane and
become vibrations.
e
The sound wave
energy is transferred
to the three bones
of the middle ear,
which vibrate.
e
The stapes is attached to
the membrane of the oval
window. Vibrations of the
oval window create fluid
waves within the cochlea.
---'r l--t:+­- ­ Vestibular duct
(perilymph)
0+-- - + - - - - Cochlear duct
(endolymph)
-,f-.,.,...--- Tympanic duct
(perilymph)
Tympanic
membrane
Round
window
The fluid waves push on the
flexible membranes of the
cochlear duct. Hair cells bend
and ion channels open,
creating an electrical signal that
alters neurotransmitter release.
• FIGURE 10-20
e
Neurotransmitter release
onto sensory neurons
creates action potentials
that travel through the
cochlear nerve to
the brain.
Cit Energy from the waves
transfers across the
cochlear duct into the
tympanic duct and is
dissipated back into
the middle ear at the
round window.
Sound transmission through the ear
open and close ion channels in the cilia membrane. When the
hair cells and cilia are in a neutral position, about 10% of the
ion channels are open, and there is a low level of tonic neuro­
transmitter released onto the primary sensory neuron.
When waves deflect the tectorial membrane so that cilia
bend toward the tallest members of a bundle, the tip links pop
more channels open, so cations (primarily K+ and Ca 2 +) enter
the cell, which then depolarizes (Fig. 1O-22b). Voltage-gated
Ca 2 + channels open, neurotransmitter release increases, and
the sensory neuron increases its firing rate. When the tectorial
membrane pushes the cilia away from the tallest members, the
springy tip links relax and all the ion channels close . Cation in­
flux slows, the membrane hyperpolarizes, less transmitter is re­
leased, and sensory neuron firing decreases (Fig. lO-22c) .
The vibration pattern of waves reaching the inner ear is
thus converted into a pattern of action potentials going to the
CNS. Because tectorial membrane vibrations reflect the fre­
quency of the incoming sound wave, the hair cells and sensory
neurons must be able to respond to sounds of nearly 20,000
waves per second, the highest frequency audible by a human ear.
CONCEPT
CHECK
17. Normally when cation channels on a cell open, either Na + or
2
Ca + enters the cell. Why is it K+ rather than Na+ that enters
hair cells when cation channels openl
Answef5: p. 383
Sounds Are Processed First in the Cochlea
The auditory system processes sound waves so that they can be
discriminated by location, pitch, and loudness. Localization of
sound is a complex process that requires sensory input from
both ears coupled with sophisticated computation by the brain
(see Fig. lO-S). In contrast, the initial processing for pitch and
loudness takes place in the cochlea of each ear.
Coding sound for pitch is primarily a function of the basi·
lar membrane. This membrane is stiff and narrow near its
THE COCHLEA
Oval
Vestibular
duct
Cochlear
duct
Organ of
Corti
Uncoiled
\
\
, ~\r
\
,
I
I
I
Round
window
Tympanic
duct
Basilar
membrane
\
Vestibular duct
,r
r "
Cochlear duct
/ ",'
(~
~
r
Tectorial membrane
/-
t.'
:
(I
A . . . . .~"-
1,
1~
~~'""~
..,--. ..
(\1, 1
Organ of Corti
The movement of the tectorial
membrane moves the cilia on
the hair cells.
Basilar
membrane
/
/
transmits action
potentials from
the hair cells to
the auditory
cortex,
/
/
Cochlear
duct
Tympanic {
duct
'
~
-
.!.l... .[- [
:-
I
..
I
::::
Nerve fibers of
cochlear nerve
• FIGURE 10-21
359
360
Chapter 10 Sensory Physiology
(a) At rest: About 10% of the ion
channels are open and a tonic signal
is sent by the sensory neuron.
Tip link
Stereocilium
r~Ul
(b) Excitation: When the hair cells bend in
one direction, the cell depolarizes, which
increases action potential frequency in
the associated sensory neuron.
Som,
channels
1open
Hair cell
~~o"
1¥6~t)
\
U'I
I
(c) Inhibition: If the hair cells bend in the
opposite direction, ion channels close,
the cell hyperpolarizes, and sensory
neuron signaling decreases.
oh,oo,',
Channels closed.
Less cation entry
hyperpolarizes cell.
open.
Cation entry
depolarizes
cell.
Primary
sensory
neuron
Action potentials
Action potentials increase
No action potentials
£
/::"
Action potentials in
primary sensory neuron
Time
0
mV
-30
Release
Membrane potential
of hair cell
e
FIGURE 10-22
Excitation opens
ion channels
Signal transduction in hair cells.
Release
Inhibition closes
ion channels
The stereocilia of hair cells
have "trap doors" that close off ion channels. These openings are controlled by
protein-bridge tiplinks connecting adjacent cilia.
attachment between the round and oval windows but widens
and becomes more flexible near its distal end (Fig. lO-23a e ) .
High-frequency waves entering the vestibular duct create
maximum displacement of the basilar membrane close to the
oval window and consequently are not transmitted very far
along the cochlea . Low-frequency waves travel along the
length of the basilar membrane and create their maximum dis­
placement near the flexible distal end . This differential re­
sponse to frequency transforms the temporal aspect of fre­
quency (number of sound waves per second) into spatial coding
for pitch by location along the basilar membrane (Fig. lO-23b).
A good analogy is a piano keyboard, where the location of a key
tells you its pitch. The spatial coding of the basilar membrane
is preserved in the auditory cortex as neurons project from hair
cells to corresponding regions in the brain.
The Ear: Hearing
Low frequency
(low pitch)
Basilar membrane
High frequency
(high pitch)
......
Stiff region near
round window
Flexible region
near helicotrema
(distal end)
(a) The basilar membrane has variable sensitivity to sound
wave frequency along its length.
Basilar
membrane
Helicotrema
Stapes
i3i~1
~~ jO~
0
10
20
30
13:~
j
o 0 0
E
(5
j
_ _ _ _:::::-_
10
20
30
:J~ I
I
o
10
20
30
- Distance from oval window (mm)­
(b) The frequency of sound waves determines the displacement
of the basilar membrane. The location of active hair celis creates
a code that the brain translates as information about the pitch
of sound.
Sensory coding for pitch takes place
along the basilar membrane. Graph adapted from G. Von
•
FIGURE 10-23
Bekesy, Experiments in Hearing (McGraw-Hili: New York, 1960).
Loudness is coded by the ear in the same way that signal
strength is coded in somatic receptors. The louder the noise,
the more rapidly action potentials fire in the sensory neuron.
Auditory Pathways Project
to the Auditory Cortex
Once the cochlea transforms sound waves into electrical sig­
nals, sensory neurons transfer this information to the brain.
The cochlear (auditory) nerve is a branch of cranial nerve VIII,
the vestibulocochlear nerve [ ~ p . 310]. Primary auditory neu­
rons project from the cochlea to cochlear nuclei in the medulla
oblongata (Fig. 10-24 e ). Some of these neurons carry informa-
361
tion that is processed into the timing of sound, and others
carry information that is processed into the sound quality.
From the medulla, secondary sensory neurons project to
two nuclei in the pons, one ipsilateral (on the same side of the
body) and one contralateral (on the opposite side). Splitting
sound signals between two ascending tracts means that each
side of the brain gets information from both ears. Ascending
tracts from the pons then synapse in nuclei in the midbrain and
thalamus before projecting to the auditory cortex (see Fig. 10-4).
Collateral pathways take information to the reticular formation
and the cerebellum.
The localization of a sound source is an integrative task
that requires simultaneous input from both ears. Unless sound
is coming from directly in front of a person , it will not reach
both ears at the same time (see Fig. 10-5) . The brain records the
time differential for sound arriving at the ears and uses com­
plex computation to create a three·dimensional representation
of the sound source.
Hearing loss May Result from Mechanical
or Neural Damage
There are three forms of hearing loss: conductive, central, and
sensorineural. In conductive hearing loss, sound cannot be trans­
mitted through either the external ear or the middle ear. The
causes of conductive hearing Joss range from an ear canal
plugged with earwax (cerumen), to fluid in the middle ear from
an infection, to diseases or trauma that impede vibration of the
malleus, incus, or stapes. Correction of conductive hearing loss
includes microsurgical techniques in which the bones of the
middle ear can be reconstructed.
Central hearing loss results either from damage to the
neural pathways between the ear and cerebral cortex or from
damage to the cortex itself, as might occur from a stroke. This
form of hearing loss is relatively uncommon.
Sensorineural hearing loss arises from damage to the struc­
tures of the inner ear, including death of hair cells as a result of
loud noises. The loss of hair cells in mammals is currently irre­
versible. Birds and lower vertebrates, however, are able to re­
generate hair cells to replace those that die. This discovery has
researchers exploring strategies to duplicate the process in
mammals, including transplantation of neural stem cells and
gene therapy to induce non sensory cells to differentiate into
hair cells.
A therapy that replaces hair cells would be an important
advance because the incidence of hearing loss in younger peo­
ple is increasing because of prolonged exposure to rock music
and environmental noises . Ninety percent of hearing loss in
the elderly-called presbycusis [presbys, old man + akoustikos,
able to be heard]-is sensorineural. Currently the primary treat­
ment for sensorineural hearing loss is the use of hearing aids,
but amazing results have been obtained with cochlear implants
attached to tiny computers (see Biotechnology box) .
r10
362
Chapter 10 Sensory Physiology
• FIGURE 10-24
pathways
Right auditory cortex
Cochlear branch of right
vestibulocochlear nerve (VIII)
Hea rin g is probably our most important social sense.
Suicide rates are higher among deaf people than among those
who ha ve lost their sight . More than any other sense, heari ng
connects us to other people and to the world around us.
BIOTECHNOLOGY
Auditory
Left auditory cortex
Cochlear branch of left
vestibu locochlear nerve (VIII)
CONCEPT
CHECK
18. Map or diagram the pathways followed by a sound wave en­
tering the ear, starting in the air at the outer ear and ending
on the auditory cortex.
19. Why is somatosensory information projected to only one
hemisphere of the brain but auditory information is projected
to both hemispheres? (Hint: See Figs. 10-5 and 10-9.)
20. Would a cochlear implant help a person who suffers from
"- . ." p.383
nerve deafness? From conductive hearing loss?
COCHLEAR IMPLANTS
One technique used to treat sensorineural hearing
loss is the cochlear implant. The newest cochlear
implants have multiple components. Externally, a micro­
phone, tiny computerized speech processor, and trans­
mitter fit behind the ear like a conventional hearing
aid . The speech processor is a transducer that converts
sound into electrical impulses. The transmitter con­
verts the processor's electrical impulses into radio
waves and sends these signals to a receiver and 8-24
electrodes, which are surgically placed under the skin .
The electrodes take electrical signa'is directly into the
cochlea and stimulate the sensory nerves. After sur­
gery, recipients go through therapy so that they can
learn to understand the sounds they hear. Cochlear
implants have been remarkably successful for many
profoundly deaf people, allowing them to hear loud
noises and modulate their own voices. In the most
successful cases, individuals can even use the tele­
phone. To learn more about cochlear implants, visit
the web site of the National Institute for Deafness
and Other Communication Disorders (www.nidcd.nih .
govlhealthlhearing) .
THE EAR: EQUILIBRIUM
Equilibrium is a state of balance, whether the word is used to
describe ion concentrations in body fluids or the position of the
body in space. The special sense of equilibrium has two compo­
nents: a dynamic component that tells us about our movement
through space, and a static component that tells us if our head
is not in its normal upright position. Sensory information from
the inner ear and from joint and muscle proprioceptors tells our
brain the location of different body parts in relation to one an­
other and to the environment, Visual information also pla ys an
important role in equilibrium, as you know if you have ever
gone to one of the 3600 movie theaters where the scene tilts sud­
denly to one side and the audience tilts with it!
Our sense of equilibrium is mediated by hair cells lining
the fluid-filled vestibular apparatus of the inner ear. These non­
neural receptors respond to changes in rotational, vertical, and
horizontal acceleration and pOSitioning. The hair cells function
just like those of the coc hlea, but gravity and acceleration
rather than sOLlnd waves provide the force that moves the
stereocilia.