Disorders of Peripheral and Central Auditory Processing
Handbook of Clinical Neurophysiology, Vol. 10
G.G. Celesia (Vol. Ed.)
# 2013 Elsevier B.V. All rights reserved
CHAPTER 1
Anatomy and physiology of the external, middle and inner ear
Sarah H. Hayesa, Dalian Dinga, Richard J. Salvia and Brian L. Allmanb,*
a
Department of Communicative Disorders and Sciences, Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo,
NY 14214, USA
b
Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, Medical Sciences
Building, London, ON, Canada
1.1. Introduction
The human auditory system represents an extraordi-
nary signal processing device, one that owes much
of its precision to a highly sensitive, biological micro-
phone found at its periphery. In order to appreciate
how environmental sound is processed in both
normal-hearing and hearing-impaired individuals, it
is necessary to understand some of the anatomical,
biomechanical, and physiological features of the
peripheral auditory system. In this chapter, we pro-
vide an overview of how acoustic energy collected
by the external ear, an oddly shaped, yet effective
funnel, is then transformed to vibratory/mechanical
energy by the three smallest bones in the body which
are encased in the middle ear. These vibrations are
finally converted to an electrical (neural) response
by an exquisite sensory epithelium consisting of pre-
cisely arranged hair cells and supporting cells housed
in the snail-like shell of the inner ear.
1.2. The external ear
The cartilaginous external ear or pinna, consisting of
the flange (outer region) and concha (deep central por-
tion), leads to the external auditory meatus or ear canal
(Fig. 1, inset). In humans, the external auditory meatus
has a length of 2–3 cm, is composed of cartilage closest
to the opening near the concha and is bony along
the remaining length until it terminates at the tympanic
membrane, or eardrum.
Although the human external ear lacks useful
musculature in comparison to other animals, it does play
*
Correspondence to: Brian L. Allman, Ph.D., Department of
Anatomy and Cell Biology, Schulich School of Medicine
and Dentistry, University of Western Ontario, Medical
Sciences Building, London, ON, Canada.
E-mail: brian.allman@schulich.uwo.ca
3
a role in both sound localization and enhancement of
sound stimulus strength particularly for high frequency
stimuli. Together, the flange and concha increase the
acoustic pressure of sounds in air over a range of
frequencies from 1.5 to 7 kHz (Fig. 1) (Gulick et al.,
1989). The flange causes a peak pressure gain of 2 dB
at 4 kHz, whereas the concha causes a peak pressure gain
of 9 dB at 5.3 kHz (Fig. 1, solid lines). Additionally, the
external auditory meatus, which is closed at one end by
the tympanic membrane, acts as an acoustic resonator
with a peak resonance at 3.3 kHz and also contributes
a maximum of 10 dB gain in pressure (Fig. 1, dashed
line). Collectively, the external ear provides approxi-
mately a 10–15 dB gain in pressure between 2 and
4 kHz (as illustrated with the unconnected dots in
Fig. 1), thereby providing effective amplification to
environmental sounds at these frequencies.
The external ear not only helps funnel sound stimuli
towards the middle ear and increases the level of sound
stimuli, but to some extent also plays a role in protecting
the tympanic membrane from the external environment.
For example, glands along the meatus produce cerumen,
or earwax, which aids in protection against foreign debris
and bacteria. An infection of the external ear (i.e., otitis
external, commonly referred to as swimmer’s ear), cau-
ses ear pain and in some cases temporary hearing loss.
1.3. The middle ear
The middle ear cavity, separated from the external ear
by the tympanic membrane, is an air-filled space
roughly 2 cm3 in volume consisting of a larger lower
portion (tympanum) and a smaller upper portion (epi-
tympanum; Fig. 2) (Gulick et al., 1989). Although the
middle ear is sealed at one end by the tympanic mem-
brane, it is open to the nasopharynx via the Eustachian
tube. This connection to the Eustachian tube allows for
equalization of pressure between the middle ear cavity
4 S.H. HAYES ET AL.

2 4 6 8 1 2 4 6 8 1
15

Flange

Pressure gain (dB)

Concha
10
Meatus

5
Concha
Meatus
Flange

0
200 500 1000 2000 5000 10,000
Frequency (Hz)
Fig. 1. Acoustic pressure gain as a function of stimulus frequency resulting from the various structures of the external ear. Solid lines depict the
pressure gain resulting from the flange and concha, and the dashed line depicts the pressure gain resulting from the meatus. The unconnected
dots represent the approximated gain in pressure resulting from the external ear (flange, concha, and meatus) and demonstrate its amplification
of mid- to high-frequency sounds. Inset depicts external ear anatomy. (From Gulick et al., 1989, with permission.)

Fig. 2. Anatomy of the middle ear cavity and ossicular chain. (From Gulick et al., 1989, with permission.)

and the external meatus. Without such an outlet,
the pressure on each side of the tympanic membrane
would be unequal causing the tympanic membrane
to vibrate abnormally. Swelling of the Eustachian
tube and middle ear cavity due to common infections,
collectively termed otitis media, can lead to the buildup
of fluid in the middle ear and an inability to equate pres-
sure (Winther et al., 2002). Otitis media is particularly
common in young children and results in ear pain as
well as temporary hearing loss (Paradise et al., 1997;
Ravicz et al., 2004).
The tympanic membrane has a cone shape which
points inward towards the middle ear. It has an area
of roughly 55–90 mm2, with the most concaved region
termed the umbo. Sound waves funneled into the mea-
tus by the external ear cause the tympanic membrane
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM
to vibrate in a complex manner; the pattern of vibra-
tion of the membrane is dependent upon both the
frequency and intensity of the sound stimulus
(Tonndorf and Khanna, 1972).
Attached to the tympanic membrane are the three
bones of the middle ear, the malleus, incus, and stapes,
together termed the ossicular chain (Fig. 2). The ossic-
ular chain is suspended within the middle ear cavity
reaching from the tympanic membrane to the inner
ear and is set in motion due to vibration of the tympanic
membrane. A number of ligaments are responsible for
suspension of the ossicular chain within the middle ear
cavity. In addition, two muscles, the tensor tympani
which attaches to the malleus and the stapedius muscle
which attaches to the stapes, influence ossicular chain
movement. The manubrium of the malleus is connected
to the central region of the tympanic membrane and is
responsible for the tympanic membrane’s conical
shape, as it pulls the tympanic membrane inward
towards the middle ear cavity. Attached to the medial
portion of the malleus, termed the head of the malleus,
is the incus. The long inferior process of the incus bends
to form its lenticular process, which is attached to the
stapes, the smallest of the three inner ear ossicles.
The medial portion of the stapes, termed the footplate,
inserts into the oval window of the inner ear. The flex-
ible annular ligament surrounding the stapes footplate
suspends it in the oval window allowing it to move
in and out like a piston.
The middle ear plays a crucial role in transmitting
acoustic stimuli collected by the outer ear from the
external environment to the sensory receptors of the
inner ear. Because fluids are less compressible than
air, an impedance mismatch exists between the air-
filled middle ear and fluid-filled inner ear. Because
of this impedance mismatch, 99.9% of sound waves
from the air would be reflected if they acted directly
on the inner ear fluids, resulting in inefficient transfer
of sound stimuli from the external environment to
the inner ear. The middle ear makes up for this imped-
ance mismatch by increasing the pressure applied to
the inner ear fluids compared to the acoustic pressure
applied to the tympanic membrane by sound stimuli.
This is accomplished in a number of ways. First,
due to the larger size of the malleus exerting force
on the shorter arm of the incus, the ossicles act as a
lever system, increasing the force applied by the stapes
at the oval window by a factor of 1.3 (Yost, 2000).
Additionally, due to the larger area of the tympanic
membrane relative to the smaller area of the stapes
footplate at the oval window, the pressure applied at
5
the oval window by the stapes footplate is 17 times
greater than the pressure at the tympanic membrane
(Yost, 2000). By measuring the gain in pressure pro-
duced by the middle ear of excised human temporal
bone samples, the peak gain in pressure has been mea-
sured in the range of 14–26.6 dB from approximately
100 to 2000 Hz and then declines at higher frequencies
(Von Bekesy, 1960; Onchi, 1961; Kurokawa and
Goode, 1995). The important function of the middle
ear in effectively transmitting sound pressure to the
inner ear is evident in patients with otosclerosis, in
which the stapes footplate is often fixed in the oval
window with little mobility, resulting in a conductive
hearing loss (Ealy and Smith, 2010).
The actions of the two middle ear muscles (i.e., ten-
sor tympani and stapedius) are thought to play a role in
regulating the transfer of acoustic pressure from the
middle ear to the inner ear. The reflexive contraction
of the muscles in response to intense sound exerts an
increased pull on the ossicles, attenuating their move-
ment and reducing the transmission of sound to the inner
ear. This middle ear reflex occurs for sounds above
80 dB and can reduce sound transmission to the inner
ear by up to 30 dB (Yost, 2000). The reflex is most
effective for low-frequency sounds below 2 kHz
and occurs with a latency of 30–150 ms following
sound exposure. Consequently, the middle ear reflex
offers protection of the inner ear against prolonged,
loud, low-frequency noise exposure (Zakrisson and
Borg, 1974; Borg et al., 1983); however, due to its
latency, the reflex offers little protection against sudden,
high-intensity sounds. The role of the stapedius muscle
in the middle ear reflex, and ultimately in attenuating
noise-induced hearing loss, is evidenced by the greater
hearing threshold shift that occurs following noise
exposure in patients suffering from Bell’s palsy, a con-
dition in which their stapedius muscle is paralyzed
(Zakrisson et al., 1975).
In addition to protection against noise over-
exposure, the middle ear muscles have also been pro-
posed to help increase the sensitivity of the inner ear
by attenuating self-generated sounds. For example,
the middle ear reflex not only occurs in response to
external sounds, but also in anticipation of self-
vocalization, which could otherwise over-stimulate
one’s inner ear (Howell et al., 1986). Furthermore,
because the middle ear reflex is most effective at atten-
uating low-frequency sounds, it is also thought to help
improve discrimination of high-frequency stimuli in the
presence of high-level, low-frequency noise that might
mask the high frequencies (Borg and Zakrisson, 1973).
6 S.H. HAYES ET AL.

The functions of the middle ear allow for the
complex vibratory patterns of the tympanic membrane
to effectively be transmitted to the inner ear. However,
due to the actions of the outer and middle ears, the sig-
nal reaching the inner ear is quite different from the
sound signal originally collected from the external
environment by the outer ear. The outer ear and exter-
nal auditory meatus amplify high-frequency sounds,
whereas the confined air of the middle ear space atten-
uates low-frequency sounds. Together, this results in a
greater sensitivity of the human ear for mid- to higher-
frequency sounds.
1.4. The inner ear
1.4.1. Gross cochlear anatomy
Having first traversed the external and middle ear,
sound stimuli then reach the inner ear where mechan-
ical pressure from the sound waves are converted to
electrical signals. Within the temporal bone lies the
bony labyrinth of the cochlea, commonly compared
to the structure of a snail shell (Fig. 3A). The bony
cochlea is a fluid-filled tube approximately 35 mm
long in humans, which coils upon itself around a cen-
tral bony core, the modiolus, producing roughly three
turns from its base to apex. The oval window, the
region of attachment of the stapes footplate, is located
in the wall of the vestibule, a larger cavity located at
the base of the cochlea. It is here where the inward
movement of the stapes, set in motion by the ossicular
chain attachment to the tympanic membrane, causes
inward and outward movements of the fluids in the
cochlea.
Located within the bony cochlear tube is a membra-
nous labyrinth (Fig. 3B). The bony cochlear tube is
divided into three fluid-filled canals: the scala
vestibuli which is continuous with the vestibule, the
scala tympani, and the scala media which lies between
the scala tympani and scala vestibuli (Fig. 4) (Raphael
and Altschuler, 2003). These canals, which spiral
along the length of the cochlea, are separated from
one another by two membranes. Reissner’s mem-
brane, which separates scala vestibuli from scala
media, reaches from the spiral limbus atop the osseous
spiral lamina, a thin bony shelf extending from the
modiolus, to the lateral cochlear wall (Fig. 5A)
(Salvi et al., 2007). The basilar membrane, which sep-
arates scala media from scala tympani, extends from
the spiral lamina to the spiral ligament at the lateral
cochlear wall. The resulting structure is a membranous
tube within the bony cochlear tube and is referred to as
the cochlear duct; enclosed on the bottom by the bas-
ilar membrane, on top by Reissner’s membrane, and
on the side by the lateral cochlear wall.
Due to the presence of a small opening, the
helicotrema, at the apex of the cochlea, the scala
vestibuli and scala tympani are able to communicate
and share the same fluid, called perilymph. The ionic
composition of perilymph is similar to that of cerebro-
spinal fluid with a high concentration of sodium (Na),
and a low concentration of potassium (K). In contrast,
the scala media of the cochlear duct contains a fluid
called endolymph which contains a high concentration
of K and a low concentration of Na, similar to that
of intracellular fluid. Running along the lateral wall
of the cochlea is a highly vascularized structure, the
stria vascularis, which plays an important role in

Fig. 3. (A) Bony inner ear of the guinea pig showing the bony cochlea as well as the vestibular semicircular canals (S). Note the location of the
oval and round windows towards the base of the bony cochlea (courtesy of D. Ding). (B) Higher magnification of the membranous labyrinth of
the guinea pig cochlea following removal of the bony cochlear walls (courtesy of D. Ding).
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM 7

Reissner’s
Membrane
Scala
Vestibuli Tectorial Lateral Wall
Scala Membrane (Apical)
Tympani Scala Media

Basilar
Membrane
(Medial)

Otic
Capsule

Spiral
Ganglion
(Rosenthal’s (Lateral)
Canal)
Cochlear Organ
(Basal)
Nerve of Corti

Fig. 4. Cross-section through the guinea pig cochlea depicting the organization of the membranous labyrinth structures within the bony
cochlear walls. (From Raphael and Altschuler, 2003, with permission.)

A B SCALA MEDIA
(Endolymph)
Scala Media (Medial) (Lateral)
Perilymph Stereocilia
ne Stria
m bra Vascularis Tectorial Membrane
me +80 mV Outer Hair
Scala Vestibuli e r’s
sn Cells Hensens
Re
is Endolymph
Cells

Outer
Hair Cells
Tectorial membrane

Spiral
Limbus Inner Spiral
Sulcus Tunnel Prominence Inner Hair 3
of
Supporting Cells Cell 1 2
Corti
Osseous Spiral
Spiral Lamina Basilar membrane Ligament

Inner Pillar Cells Scala Tympani

Spiral Ganglion Hair Cells
Cells Habenula
Perforata Perilymph

Fig. 5. (A) Diagram of the cochlear duct depicting the location and cellular composition of the organ of Corti. (From Salvi et al., 2007, with
permission.) (B) Cross-section through the mole rat cochlea showing a higher magnification view of the organ of Corti. Note the attachment of
the outer hair cell stereocilia, but not the inner hair cell stereocilia, to the overlying tectoral membrane. (From Raphael and Altschuler, 2003,
with permission.)

generating the ionic composition of the endolymph of the round window membrane into the middle ear
found in the scala media (Wangemann, 2006). cavity relieves pressure in the cochlear fluid generated
An additional membrane-covered opening, the round by the inward movement of the oval window. The pres-
window, is located at the base of the cochlea where sure fluctuations generated in perilymph by the action
the scala tympani terminates. The outward movement of the stapes footplate at the oval window travel through
8 S.H. HAYES ET AL.

the scala vestibuli towards the apex and helicotrema
and continue through to scala tympani, ultimately caus-
ing outward movement of the round window.
1.4.2. Organ of Corti
Resting on top of the basilar membrane, and running
the length of the cochlear duct within the scala media,
is the sensory organ of the cochlea, the organ of Corti
(Fig. 5). The organ of Corti contains two types of sen-
sory hair cells, the inner and outer hair cells, as well as
a number of supporting cell types. The inner and outer
pillar cells form a tunnel structure through the center
of the organ of Corti termed the arch of Corti, in which
inner hair cells lie medial to the inner pillar cells clos-
est to the modiolus, and outer hair cells lie lateral to the
outer pillar cells closest to the lateral cochlear wall.
The human cochlea contains about 3000 inner hair
cells that are organized in a single row running along
the length of the basilar membrane, and about 12,000
outer hair cells that run in three parallel rows.
A gelatinous structure called the tectoral membrane
extends from the spiral limbus and rests on top of
the organ of Corti in the scala media. The remaining
supporting cells in the organ of Corti, such as cells
of Dieters, Hensen, Claudius, and Boettcher, provide
additional structural support and assist in holding
the hair cells in place.
1.4.3. Cochlear hair cells
As the sensory receptors for the inner ear, hair cells
have a specialized structure which allows them to
detect the movement of cochlear fluids generated by
the middle ear ossicles. Along the apical surface of
the hair cells is a fibrous network of actin, myosin
and fimbrin, together forming the cuticular plate, from
which specialized stereocilia emerge (Fig. 6). Stereo-
cilia are composed of polymerized actin filaments
(Flock and Cheung, 1977) and are arranged in a
stair-step pattern, with the shortest row facing the
modiolus and the tallest row closest to the lateral
cochlear wall. The stereocilia have a uniform thick-
ness for much of their length, but taper at the point

A C

OHC

IHC

B (Lateral)
R

Outer Hair
Cell

Pillar Cells (Roof of

Tunnel) Stereocilia

Inner Hair Cell

(Medial) 2.5 µm

Fig. 6. (A) Scanning electron micrograph showing the organization of the stereocilia bundles on the three rows of outer hair cells (OHC) and
single row of inner hair cells (IHC) in the chinchilla cochlea (courtesy of D. Ding). (B) Higher magnification scanning electron micrograph
showing the organization of the stereocilia bundles on inner and outer hair cells. Note the stair-step organization of stereocilia, with two major
rows of stereocilia seen on inner hair cells and three organized rows of stereocilia on outer hair cells. (From Raphael and Altschuler, 2003, with
permission.) (C) Transition electron microscopy (TEM) image of guinea pig cochlear hair cell stereocilia. Tip links (at arrows) as well as side
links (R) can be seen connecting adjacent stereocilia. (From Furness et al., 2008, with permission.)
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM
of attachment to the cuticular plate, thereby providing
the stereocilia with the ability to pivot and bend near
the base. Each of the pear-shaped inner hair cells has
about 40 cilia organized in two rows forming a slight
“U” shape, whereas each of the cylindrically shaped
outer hair cells has about 150 cilia organized in three
rows forming a “V” or “W” shape (Fig. 6A and B).
The tallest of the stereocilia on each outer hair cell
is firmly imbedded in the overlying tectoral mem-
brane. Fine fibrils, called cross-links, couple adjacent
stereocilia together so that the stereocilia on each hair
cell move together as a unit (Osborne et al., 1984;
Pickles et al., 1984; Furness et al., 2008) (Fig. 6C).
Another form of fibril, the tip-link, connects the shaft
of one stereocilia to the tip of an adjacent shorter
stereocilia (Pickles et al., 1984). These tip-links are
associated with mechanically gated ion channels in
the stereocilia membrane and play an important role
in hair cell transduction. Electrophysiological evi-
dence suggests that the mechanically gated ion chan-
nels associated with tip links are located near the tips
of the hair cell stereocilia. For example, by measuring
the extracellular voltage at different points along the
length of the hair cells, it was found that the largest
voltage steps in response to stereocilia deflection
occurred near the tip of the hair cell bundle (Russell
and Sellick, 1978; Hudspeth, 1982).
1.4.4. Hair cell transduction
The function of the cochlear hair cell is to convert
mechanical vibration induced by sound waves into
electrical signals that are transmitted to the brain via
the auditory portion of the VIII cranial nerve. The
movement in the inner ear fluids produced by the
action of the stapes footplate results in vibration of
the basilar membrane, which in turn causes the stereo-
cilia of the inner and outer hair cells to be deflected.
When the stereocilia are deflected towards the tallest
of the stereocilia, tension in the tip links pull the asso-
ciated mechanically gated ion channels open allowing
positively charged ions (mainly K from the endolymph)
to flow into the hair cell, thereby causing the hair cell to
become depolarized (Fig. 7). However, when stereo-
cilia are deflected in the opposite direction, the mechan-
ically gated ion channels close causing the hair cell to
hyperpolarize. The resulting change in intracellular
potential is called the hair cell receptor potential.
When inner hair cells are depolarized they respond
by releasing neurotransmitters at their basal surface
thereby activating the auditory nerve fibers onto which
9
they synapse, ultimately allowing an electrical signal
to be propagated to the central auditory structures of
the brain. Outer hair cells, on the other hand, respond
to depolarization and hyperpolarization by altering
their cellular shape (Brownell et al., 1985; Ashmore,
1987). They shorten and lengthen along their longitu-
dinal axis with an overall length change of
2 mm
(Ashmore, 1987). The “electromotile” properties of
outer hair cells allow them to function as mechanical
amplifiers; by altering their shape in response to stim-
ulation, they further enhance the vibration of the bas-
ilar membrane leading to greater activation of adjacent
inner hair cells. The vibration of the basilar membrane
induced by outer hair cells has been observed in
excised cochleae (Mammano and Ashmore, 1993).
By stimulating the organ of Corti with an electrical
current, place-specific vibrations of the basilar mem-
brane could be measured in the region in which the
organ of Corti was stimulated.
Prestin has been identified as the outer hair cell
motor protein responsible for outer hair cell motility
(Zheng et al., 2000) (Fig. 8). The plasma membrane
of outer hair cells, which contains a dense network of
intramembranous proteins, as well as wrinkles which
allow for cellular elongation and contraction, contains
numerous prestin molecules (Forge, 1991; Oghalai
et al., 1998; Chen et al., 2009). Prestin undergoes a con-
formational change in shape that reduces the length of
outer hair cells when they become depolarized and
increases outer hair cell length in response to hyperpo-
larization (Ashmore, 1987, 2008; Santos-Sacchi and
Dilger, 1988). The prestin molecule itself contains a
voltage sensor which is sensitive to the intracellular
concentration of chloride and bicarbonate anions
(Oliver et al., 2001). In response to changes in trans-
membrane voltage, prestin undergoes a structural
rearrangement, resulting in the alteration of outer hair
cell shape. Deletion of the gene encoding for prestin
in mice results in a loss of outer hair cell electromotility
and a hearing loss of 40–60 dB (Liberman et al., 2002).
The electromotility of outer hair cells is believed to
underlie the otoacoustic emissions recorded from the
ear, which are low-intensity sounds produced by the
inner ear either spontaneously or in response to sound
stimulation (Kemp, 1978; Brownell, 1990). The vibra-
tion of the basilar membrane generated by the outer
hair cells produces movements in the cochlear fluids
which are transmitted back to the stapes footplate
and then to the tympanic membrane. Otoacoustic
emissions provide a method of assessing outer hair cell
function as they reflect the electromotility of outer hair
10 S.H. HAYES ET AL.

Radial shear creates tension on tip link

High K+ High K+
+80 mV +80 mV
Mechanically-
gated channel

−45 to [K+]
−70 mV
Depolarization

Depolarization Hyperpolarization

Inhibition
Receptor
Potential
Excitation

Fig. 7. Schematic diagram depicting the hair cell transduction process. When hair cell stereocilia are deflected in the direction of the tallest
stereocilium, mechanically gated ion channels associated with the tip links open allowing potassium ions from the endolymph to flow into the
hair cell resulting in the depolarization of the hair cell. In contrast, deflection of stereocilia in the opposite direction closes the mechanically
gated ion channels resulting in hyperpolarization of the hair cell. (From Salvi et al., 2007, with permission.)

cells. Recording the otoacoustic emissions by placing
a sensitive microphone probe in the ear canal is a
common method for assessing auditory function
particularly in infants. The crucial role of prestin in
generating outer hair cell electromotility and therefore
otoacoustic emissions is evident in prestin knockout
mice, which in addition to lacking outer hair cell
electromotility also lack otoacoustic emissions
(Liberman et al., 2002).
1.4.5. Hair cell innervation: afferent system
The different response of inner and outer hair cells to
activation is reflected in their pattern of innervation by
auditory nerve fibers of the eighth cranial nerve, which
transmits neural activity from the cochlea to the cen-
tral auditory system (Fig. 9) (Spoendlin, 1978). The
spiral ganglion neurons of the auditory nerve are bipo-
lar neurons; their peripheral process synapses on
cochlear hair cells and their central process projects
to the cochlear nucleus of the brainstem. The periph-
eral process of the auditory nerve fibers pass through
small openings in the osseous spiral lamina called the
habenula perforata to innervate hair cells of the organ
of Corti. There are two types of auditory nerve fibers
type I and type II. Type I fibers make up 90–95% of all
auditory nerve fibers and each synapses on a single
inner hair cell, with each inner hair cell being con-
tacted by many type I fibers. In response to inner hair
cell activation by sound stimuli, type I fibers fire
action potentials which are transmitted to the central
auditory system. Type II fibers make up the remaining
5–10% of auditory nerve fibers; each of these fibers
branches to contact multiple outer hair cells. However,
these nerve fibers do not appear to fire action poten-
tials in response to sound stimuli (Robertson, 1984).
Although there are nearly three times as many outer
hair cells as inner hair cells, the outer hair cells receive
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM 11

A B

longitudinal plasma
force ~ 0.1nN/µm membrane

Vm OHC 3 2 1 IHC

Vm

30 nm

10µm
cytoskeleton motor
particles

Fig. 8. (A) Diagram of the mechanism proposed to underlie the electromotile properties of outer hair cells (OHCs). Motor proteins within the
OHC membrane alter the longitudinal length of OHCs in response to changes in membrane potential. Hyperpolarization (Vm #) results in an
increase in OHC length, whereas depolarization (Vm ") leads to a reduction in OHC length. (From Ashmore, 2008, with permission.)
(B) Fluorescent image of a rat cochlea in which nuclei (red) and prestin (green) have been labeled. Prestin, the motor protein responsible
for OHC electromotility, is specifically expressed in the OHC membrane and is absent from inner hair cells (IHCs). (From Chen et al.,
2009, with permission).

Apex
OHC Base

IHC

Type II
ha

Type I

sg

AN

to CN
Fig. 9. Afferent innervation pattern of the cochlea by auditory nerve (AN) fibers. Spiral ganglion (sg) neurons of the AN send their peripheral
process through the habenula perforata (ha) of the osseus spiral lamina to innervate the organ of Corti. Type I fibers innervate inner hair cells
(IHC) while a lesser number of Type II fibers innervate outer hair cells (OHC). (Adapted from Spoendlin, 1978.)

little afferent innervation by auditory nerve fibers. The fibers, whereas outer hair cells mainly function by
inner hair cells, which are mainly responsible for increasing the sensitivity of inner hair cells via
transmitting mechanical stimulation into electrical mechanical amplification of incoming sound
signals, synapse with many more auditory nerve vibrations.
12
1.4.6. Hair cell innervation: efferent system
In addition to the afferent innervation of cochlear hair
cells by auditory nerve fibers, hair cells also receive
efferent inputs originating from the superior olivary
complex of the auditory brainstem (Liberman, 1990;
for review see Guinan, 2006) (Fig. 10). Both the medial
superior olive (MSO) and the lateral superior olive
(LSO) provide fibers which combine to form the
olivocochlear efferent fibers. Fibers originating from
the MSO are termed medial olivocochlear (MOC) effer-
ents, and those originating from the LSO are termed lat-
eral olivocochlear (LOC) efferents. MOC and LOC
efferents project to both the ipsilateral (uncrossed) and
contralateral (crossed) cochlea; however, more MOC
fibers project contralaterally, while LOC fibers predom-
inantly project ipsilaterally to the cochlea. Together, the
ipsilateral and contralateral MOC and LOC efferent pro-
jections combine to form the olivocochlear bundle
(OCB) which enters the cochlea as the intraganglionic
spiral bundle. LOC efferents primarily terminate on
the dendrites of type I auditory nerve fibers which con-
tact the inner hair cells, while MOC efferents primarily
terminate directly on outer hair cells. MOC efferents, due
to their connection with outer hair cells, are believed to
play a role in protecting the ear from damage caused by
acoustic overstimulation by modulating the motility of
4th Ventricle
Crossed
Efferents
CN LOC
Efferents
Uncrossed
Efferents
LSO
MOC
Efferents
MSO
Fig. 10. Efferent innervation pattern of the cochlea by the auditory brainstem. Crossed and uncrossed fibers from the lateral and medial supe-
rior olives give rise to the olivocochlear bundle (OCB) whose efferents enter the cochlea with the AN after crossing over from the inferior
vestibular nerve at Oort’s vestibulocochlear anastomosis, the junction between the vestibular and auditory nerves. CN ¼ cochlear nucleus;
LOC ¼ lateral olivocochlear; LSO ¼ lateral superior olive; MOC ¼ medial olivocochlear; MSO ¼ medial superior olive. (Adapted from
Liberman, 1990, with permission.)
S.H. HAYES ET AL.
outer hair cells. When the fibers of the crossed (contra-
lateral) OCB predominately containing MOC fibers
are stimulated, both basilar membrane motion and inner
hair cell receptor potentials are reduced, suggesting that
the MOC fibers are able to influence cochlear sensitivity
by modulating outer hair cell electromotility (Brown and
Nuttall, 1984; Murugasu and Russell, 1996). To date,
much less is known about the role of LOC efferents,
although they are also suggested to protect the inner
ear from acoustic overexposure. It is thought, due to their
direct connections with auditory nerve dendrites, that
LOC efferents may protect type I auditory nerve fibers
from excitotoxicity resulting from acoustic overexpo-
sure. By stereotaxically destroying LOC cell bodies in
the mouse brainstem, it was found that the ear ipsilateral
to the lesion had greater threshold shifts following
acoustic overexposure compared to contralateral ears,
suggesting that the ipsilateral LOC efferents indeed play
a role in protecting the cochlea from acoustic trauma
(Darrow et al., 2007).
1.4.7. Cochlear mechanics
As noted above, sound-induced movement of the bas-
ilar membrane leads to the activation of hair cells.
Much of what we know about the vibration of the bas-
ilar membrane originates from the pioneering studies
OCB
CN
LOC AN
Efferents
Vestibulo-Cochlear
Anastomosis (Oort)
Cochlea
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM
conducted by George von Bekesy who first described
the characteristic movements of the basilar membrane
by observing excised temporal bone specimens from
cadavers (von Bekesy, 1947). Because the fluids of
the inner ear are nearly incompressible, the inward
movement of the stapes footplate causes the fluctua-
tion of cochlear fluids to occur nearly instantaneously
along the entire length of the cochlea. However, the
basilar membrane does not move in unison along its
entire length. From base to apex, the stiffness of the
basilar membrane gradually decreases, while its width
(and mass) increases. This difference in physical prop-
erties along the length of the basilar membrane results
in the stiffer and lighter base vibrating earlier than the
apex when fluid fluctuations are generated by the sta-
pes footplate. In effect, when fluid fluctuations are
generated by the stapes, vibration of the basilar mem-
brane begins at the base and propagates towards the
apex generating what appears as a “traveling wave”
(Fig. 11). The gradient of stiffness and mass along
the length of the basilar membrane also accounts for
its frequency-specific movement. High-frequency
sounds produce maximal displacement of the basilar
membrane at the base of the cochlea, whereas low-
frequency sounds produce maximal displacement at
the apex. Although low-frequency sounds produce
maximal displacement at the apex of the basilar mem-
brane, they also produce displacement at the base due
to the traveling wave’s progression from the base to
the apex. However, high-frequency sounds only pro-
duce displacement at the base. This variation in region
specific displacement leads to a frequency-to-place
representation in the cochlea, with high-frequency
Base
Low
frequency
Mid
frequency
High
frequency
Fig. 11. Schematic diagram depicting the traveling wave displacement pattern of the basilar membrane. Low-frequency stimuli produce max-
imal displacement at the apex of the basilar membrane, mid-frequency stimuli produce maximal displacement in the middle regions of the
basilar membrane, and high-frequency stimuli cause maximal displacement at the base of the cochlea. Dashed lines represent the envelope of
the basilar membrane response. Unlike low-frequency stimuli which produce displacement of the base and apex of the basilar membrane, high-
frequency stimuli only produce displacement at the base.
13
sounds producing maximal activation of hair cells at
the base of the cochlea and low-frequency sounds
maximally activating hair cells at the apex of the
cochlea. In fact, the frequency-specific displacement
of the basilar membrane is very sharply tuned.
By monitoring the displacement of a region of the bas-
ilar membrane near the base of the cochlea in response
to different frequencies and intensities of sound, we can
obtain a frequency tuning curve for that specific region
(Fig. 12A). The frequency with the lowest threshold, or
lowest intensity required to cause a measurable dis-
placement of the basilar membrane, is termed the char-
acteristic frequency (CF) for that region. In the region
near the base of the cochlea depicted in Fig. 12A, the
CF is close to 10 kHz and can be seen as the sharply
tuned tip of the tuning curve. Frequencies greater and
less than the CF have higher thresholds; frequencies
below CF have high thresholds resulting in a broadly
tuned “tail” below CF. The basilar membrane response
to increases in sound intensity near CF is also character-
ized by compressive non-linearity. That is, when stim-
ulated with a sound at or near the CF for a given region
of the basilar membrane, the displacement of the basilar
membrane increases with increasing stimulus intensi-
ties, but saturates at higher intensities. Stimulation with
frequencies above or below the CF, however, results in
close to a linear relationship between basilar membrane
movement and stimulus level.
1.4.8. Hair cell tuning
How is the mechanical tuning of the basilar membrane
related to the activation of hair cells at different
Uncoiled cochlea Apex
Helicotrema
Basilar Membrane
14 S.H. HAYES ET AL.

A
90
80
70
60

dB SPL
50
40
30
Amplitude
20
10
0
100 1000 10000 100000
Frequency (Hz)

B
90
80
Sound Intensity (dB SPL)

70
60
50
40
IHC
30 OHC
20
10
0
1 3 5 10 30
Frequency (kHz)
Fig. 12. (A) Representative frequency–threshold tuning curve for a region of the basilar membrane near the base of the cochlea, demonstrating
the sharply tuned displacement pattern of the basilar membrane. (B) Receptor potential tuning curves for an inner (IHC) and outer hair cell
(OHC). (From Cody and Russell, 1987, with permission.) Note the similarity between basilar membrane and hair cell tuning curves.

regions along the basilar membrane? By using sharp
microelectrodes, the activity of individual hair cells
can be recorded under resting conditions and in
response to sound stimulation (Russell and Sellick,
1977). The resting membrane potential of inner hair
cells ranges from 40 to 50 mV, while that of the
outer hair cells is around 70 mV (Cody and Russell,
1987). The tuning curves of inner and outer hair cells
at a location near the base of the cochlea are shown in
Fig. 12B. The sound intensity required to produce a
measurable response from the cells is plotted over a
range of frequencies. Similar to the tuning curve for
the basilar membrane, the tuning curves of inner and
outer hair cells have a low threshold, sharply tuned
tip representing the cell’s characteristic frequency,
and a high threshold, broadly tuned tail. The similarity
between the tuning curves of hair cells and the basilar
membrane suggests that the mechanical response of
the basilar membrane is faithfully transmitted to the
hair cells.
1.4.9. Inner and outer hair cell loss
Animal studies in which either inner or outer hair cells
have been selectively destroyed have demonstrated
the distinct roles of the two types of cochlear hair cell.
These studies also elucidate some of the underly-
ing mechanisms of sensorineural hearing loss (i.e.,
hearing loss resulting from conditions affecting the
auditory nerve or inner ear). Common causes of sen-
sorineural hearing loss (SNHL) include noise-induced
inner ear damage, ototoxicity due to chemotherapy
agents or antibiotics, auditory neuropathy, and pres-
bycusis (age-related hearing loss).
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM 15

Disruption of inner hair cells and their associated A

auditory nerve fibers has dramatic effects on auditory
functioning and is believed to underlie the hearing dis-
order known as auditory neuropathy. Auditory neu-
ropathy, which accounts for 2.4–15% of SNHL
cases, is believed to be the result of either damage
to inner hair cells, the synapse between inner hair cells OHC
and auditory nerve fibers, or to auditory nerve fibers
themselves (Starr et al., 1996). Patients suffering from IHC
this disorder have normal outer hair cell function, as
measured by otoacoustic emissions, but abnormal
auditory brainstem responses and hearing deficits such
as poor speech discrimination particularly in noisy
environments. In an attempt to better understand the
distinct roles of inner and outer hair cells, as well as
disorders such as auditory neuropathy, animal models B
of selective inner hair cell and spiral ganglion neuron
loss have been developed. Administration of the
chemotherapy agent carboplatin to chinchillas pro-
duces selective damage to inner hair cells and
spiral ganglion neurons leaving the majority of outer
OHC
hair cells intact and functioning (Wang et al., 1997,
2003) (Fig. 13A). In the auditory nerve fibers that
IHC
are left intact, sharpness of tuning and low thresholds
at near CF are retained, thus demonstrating the role of
functional outer hair cells in the sensitivity and tuning
of the cochlea. However, both spontaneous and driven
discharge rates are reduced indicating that selective
inner hair cell damage dramatically affects the trans-
mission of information to the central auditory brain Fig. 13. (A) Photomicrograph of a cochlear preparation from a chin-
by the auditory nerve. chilla exposed to the ototoxic agent carboplatin which selectively
Various agents such as the antibiotic kanamycin destroys inner hair cells (IHC) while leaving outer hair cells
and acoustic overexposure have been utilized to selec- (OHC) intact. Arrows indicate regions of missing inner hair cells.
(B) Photomicrograph of a cochlear preparation from a chinchilla
tively destroy outer hair cells. Loss of outer hair cells
exposed to intense noise. Notice the selective loss of OHCs while
results in an elevation of auditory thresholds as high as most IHCs are left intact. (courtesy of D. Ding)
60 dB, as well as poor frequency selectivity evidenced
by the widening of frequency tuning curves (Ryan and
Dallos, 1975; Dallos and Harris, 1978; Liberman and cell stereocilia can also lose their attachments to the
Kiang, 1978). These results further demonstrate the overlying tectorial membrane (Fig. 14).
role of outer hair cells in cochlear tuning and sensitiv-
ity. In addition to ototoxic agents, intense noise also
1.5. Cochlear potentials
causes hair cell damage. Although intense noise expo-
sure has devastating effects on many cochlear cell 1.5.1. The endocochlear potential
types, it is the outer hair cells that appear to be the most
vulnerable (Henderson et al., 2006). In fact, it is the Early studies conducted by von Bekesy were some of
damage of outer hair cells following noise exposure the earliest to investigate the electrochemical properties
that significantly contributes to noise-induced hearing of the fluid-filled spaces of the cochlea (von Bekesy,
loss. Loss of outer hair cells via apoptosis and necrosis 1951). By advancing an electrode through the cochlea,
can produce cochlear lesions following noise exposure he was able to record the changes in electrical potentials
(Fig. 13B). Additionally, intense noise exposure can of the different fluid-filled cochlear regions. Record-
damage hair cell stereocilia and tip-links; outer hair ings from the scala tympani demonstrate that the
16
Fig. 14. Scanning electron micrograph of a guinea pig cochlea
showing (A) normal outer hair cell stereocilia organization and
(B) dramatic damage to outer hair cell stereocilia following intense
noise exposure (courtesy of D. Ding).
perilymph has a þ7 mV electrical potential (Johnstone
and Sellick, 1972). As stated previously, the resting
potential recorded from inner hair cells is 40 to
50 mV, whereas that of outer hair cells is 70 mV
(Dallos et al., 1982; Cody and Russell, 1987). When
an electrode is passed into the scala media, a dramatic
increase in the electrical potential is recorded. This
potential, referred to as the endocochlear potential, is
þ80 mV and exists in the absence of acoustic stimuli
(Peake et al., 1969; Bosher and Warren, 1971)
(Fig. 15A). In fact, the endocochlear potential is the
largest transepithelial voltage in the human body
(Wangemann, 2006), and is the driving force for hair
cell transduction. The striking 125–150 mV potential
difference between the hair cells and endolymph is
what drives the influx of K ions into the hair cells fol-
lowing the opening of mechanically gated ion channels
in the stereocilia. Thus, the endocochlear potential is
vital for the transduction of sound waves into nerve
impulses by the hair cells.
1.5.2. The stria vascularis and potassium cycling
Originally, the endocochlear potential was thought to
originate from the ionic concentration gradient
between the endolymph and perilymph. However,
altering the concentration of K within the perilymph
has little effect on endocochlear potential amplitude
(Tasaki et al., 1954). Further investigation revealed
that the stria vascularis, the highly vascularized region
of the lateral cochlear wall, is responsible for generat-
ing the ionic composition of endolymph as well as the
endocochlear potential (for review, see Wangemann,
S.H. HAYES ET AL.
2006, 2008). The stria vascularis has a layered epithelial
structure, diagrammed in Fig. 15B. On their medial
surface, strial basal cells are connected to intermedi-
ate cells via gap junctions whereas on their lateral sur-
face, basal cells connect to fibrocytes of the spiral
ligament by another set of gap junctions. The gap
junctions allow fibrocytes, basal cells and intermedi-
ate cells to be electrically coupled and permit ions and
small molecules to flow between these cells. On the
surface of the stria vascularis lining the scala media
are strial marginal cells which are separated from
intermediate cells by intrastrial fluid.
Several ion transport mechanisms within the stria
vascularis contribute to the generation of the
endocochlear potential by recycling K from the endo-
lymph. K ions that enter the stereocilia during trans-
duction flow through the hair cells to the perilymph,
through the spiral ligament, and back to the stria
vascularis where it is once again released back into
the endolymph (Fig.15A, solid arrows). K ions leave
the hair cells via basolateral K channels out into the
perilymph where they are then taken up by fibrocytes
of the spiral ligament. Additionally, K ions in the
endolymph also enter the perilymph of the scala ves-
tibuli directly through Reissner’s membrane where
they are then taken up by fibrocytes. Once in the
fibrocytes, K is able to diffuse through the strial basal
cells to the strial intermediate cells due to the presence
of gap junctions, causing the intermediate cells to have
a high concentration of K ions. K channels (Kcnj10,
Kir 4.1) located in the membrane of intermediate
cells allow for K ions to diffuse down their concentra-
tion gradient into the intrastrial space which has a
relatively low K concentration. The ionic K concentra-
tion is kept low within the intrastrial space due to the
action of a number of transport mechanisms in the
marginal cell membrane. A Na-2Cl-K cotransporter
(Slc12a2) and the Na,K-ATPase (Atp1a1/Atp1b2)
allow for K ions to be taken up by the marginal cells
from the intrastrial fluid. Once in the marginal cells,
K ions are then secreted back into the endolymph of
the scala media by the K channel Kcnq1/Kcne1.
Fig. 15B shows a detailed diagram of the transport
mechanisms within the stria vascularis giving rise to
the endocochlear potential. In essence, the major driv-
ing force for the generation of the endocochlear poten-
tial is the large potential difference between the
intrastrial fluid and the intermediate cell
(Wangemann, 2002, 2006). In combination, the
uptake of K from the intrastrial space by the marginal
cells and the diffusion of K into the intermediate cells
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM 17

Perilymph Scala Media

ne Stria
mbra Vascularis
me +80 mV
Scala Vestibuli r’s
ne Endolymph
iss
Re
K+
Outer
Hair Cells
Tectorial membrane

Spiral
Spiral
Inner Prominence
Limbus
Sulcus Tunnel
of Spiral
Corti Supporting Cells
Ligament
Osseous
Spiral Lamina Basilar membrane

Inner Pillar Cells Scala Tympani

Spiral Ganglion
Hair Cells
Cells Habenula
Perforata
Perilymph
B

ATP1A1 ATP1A1
ATP1B2 ATP1B2
Na+ K+ Na+
GJB2
KCNQ1 K+ Na+ K+
GJB6
KCNE1
CLCNKA
K+ Cl− K+ Cl−
CLCNKB
BSND KCNJ10
K+ Na+
Na+ K+
2Cl−
2Cl−
Intermediate K+
K+
Cells SLC12A2
SLC12A2
Fibrocyte
Marginal Intrastrial space Basal
80 mV Cells 90 mV Cells 0 mV

Endolymph Stria Vascularis Spiral

Ligament
Fig. 15. The stria vascularis is the source of the endocochlear potential. (A) Schematic diagram showing the flow of potassium ions into the
endolymph and then back to the stria vascularis through the basilar and Reissner’s membrane. (From Salvi et al., 2007, with permission.)
(B) Magnified representation of the stria vascularis depicting the numerous transport mechanisms involved in the generation of the
endocochlear potential. (Adapted from Wangemann, 2008, with permission.)

from fibrocytes of the spiral ligament contribute to the malfunction of the complex transport mechanisms
diffusion of K ions down their concentration gradient within the stria vascularis has dramatic effects on
via Kcnj10 (Kir 4.1) channels, which ultimately cochlear function. Mutations in Kcnq1 and Kcne1,
produces the þ80 mV endocochlear potential. the channels involved in secretion of K from
Because the endocochlear potential is so important marginal cells into the endolymph, underlie
for hair cell transduction, it is not surprising that Jervell and Lange–Nielsen syndromes which are
18 S.H. HAYES ET AL.

characterized by profound deafness (Schulze-Bahr 1.5.3. Evoked cochlear potentials

et al., 1997; Wang et al., 2002). Similarly, inhibition
of Slc12a2, the marginal cell Na-2Cl-K cotransporter,
results in a loss of the endocochlear potential and the
collapse of the endolymphatic space (Kusakari et al.,
1978). Deletion of Kcnj10, the K channel most impor-
tant for endocochlear potential generation by allowing
for the movement of K from the intermediate cells to
the intrastrial fluid, also results in the loss of the
endocochlear potential (Marcus et al., 2002). Addition-
ally, mutation in the genes encoding for gap junction
proteins, including Gjb2 and Gjb6, underlie hereditary
cases of childhood deafness and deletion of the Gjb6
gene in mice results in deafness and the loss of the
endocochlear potential (Zelante et al., 1997; Del
Castillo et al., 2003; Teubner et al., 2003). Gap junc-
tions are not only important for electrical coupling of
cochlear cells, but also appear to be important for the
passage of metabolites between cochlear cells (Zhang
et al., 2005; Matsunami et al., 2006).
In addition to the resting potentials of the inner ear (the
endocochlear potential and the hair cell resting poten-
tials) three sound-evoked potentials, the cochlear micro-
phonic, summating potential, and the compound action
potential, are also generated in the inner ear (Fig. 16).
In response to sound stimuli these potentials can be
recorded from electrodes placed in the cochlea or at loca-
tions outside the cochlea such as at the round window.
1.5.3.1. Cochlear microphonic
When an electrode is placed on or near the cochlea, an
alternating current (AC) response, called the cochlear
microphonic (CM), can be observed when sound stim-
uli are presented (Fig. 16B). The frequency of this AC
response closely mimics the frequency of the sound
stimulus, demonstrating the ability of the cochlea
to act as a “microphone” by transducing sound
stimuli into comparable oscillations in voltage

A B
400 400
Cochlear Microphonic
300 300

200 200
Amplitude (mV)

Amplitude (mV)

100 100

0 0

−100 −100

−200 −200

−300 −300

−400 −400
0 5 10 15 0 5 10 15
Time (ms) Time (ms)

C D
Summating Potential Compound Action Potential
100 100 onset offset
Amplitude (mV)

Amplitude (mV)

SP

0 0
2
N

−100 −100
1
N

0 5 10 15 0 5 10 15
Time (ms) Time (ms)
Fig. 16. Evoked potentials recorded from the rat cochlea. (A) Unfiltered recording from the cochlea in response to a noise burst. (B) Cochlear
microphonic (CM) isolated by filtering the cochlear response in A. The CM is seen as an alternating current response. (C) Summating potential
(SP) isolated from the cochlear response in A, showing the SP as a direct current shift. (D) Compound action potential (CAP) isolated from the
cochlear response in A. The two predominant negative peaks of the CAP (N1 and N2) are shown. (courtesy of G.D. Chen)
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM 19

(Wever and Bray, 1930). For example, the CM will
appear as a 1 kHz electrical sinusoidal wave if the
ear is stimulated with a 1 kHz tone. The amplitude
of the CM varies with the intensity of the sound stim-
ulus, with the amplitude increasing linearly with
increasing stimulus levels from low to mid intensities,
and eventually saturates and declines with very high-
intensity stimuli (Fig. 17A). The CM also varies with
frequency, closely following the frequency-to-place
displacement of the basilar membrane. High-
frequency stimuli produce a CM at the base of the
cochlea but not at the apex, while low-frequency stim-
uli produce a CM at both the base and apex, similar to
the basilar membrane’s traveling wave. It is now
known that the CM is the result of receptor currents
flowing through the hair cells, which explains the
close relationship between the CM and displacement
of the basilar membrane which is responsible for hair
cell activation (Tasaki et al., 1954; Dallos et al., 1972;
Dallos and Cheatham, 1976).
Studies in which inner or outer hair cells have been
selectively destroyed have demonstrated that it is the
outer hair cells which are the dominant contributors to
the CM. For example, selective destruction of outer
hair cells with kanamycin results in a dramatic reduc-
tion of the CM (Dallos and Wang, 1974). However,
selective destruction of inner hair cells or the auditory
nerve has little effect on the CM (Trautwein et al.,
1996; XY Zheng et al., 1997).
1.5.3.2. Summating potential
In addition to the CM, a step-like direct current (DC)
shift can also be recorded from the inner ear in
response to sound stimuli (Fig. 16C). This DC
response, called the summating potential (SP), lasts
for the duration of the sound stimulus and is positive
or negative depending on the parameters of the stim-
ulus as well as the recording site (Dallos et al., 1970).
Unlike the CM which has a more broadly tuned
response to sound stimulation with various frequen-
cies, the SP is more narrowly tuned. The SP is negative
near the characteristic frequency for a given region of
the cochlea, but reverses polarity at frequencies above
and below the characteristic frequency.
It is currently believed that the inner hair cells con-
tribute significantly to the SP. Selective destruction of
type I afferent neurons and inner hair cells by round win-
dow application of kainic acid or sectioning of the audi-
tory nerve in chinchilla results in a dramatic decrease in
the amplitude of the SP recorded at the round window
with little effect on the CM (Fig. 17B) (Zheng et al.,
1997). Likewise, destruction of inner hair cells and

A B
1000
1000 Control
IHC Loss
IHC + OHC Loss
CM Amplitude (uV)

SP Amplitude (uV)

100 100

10 10

1 1
0 20 40 60 80 100 0 20 40 60 80 100
dB SPL dB SPL
Fig. 17. (A) Cochlear microphonic (CM) amplitude as a function of stimulus intensity. At low to mid frequencies the amplitude increases
linearly with increasing intensities but saturates at high intensities. (B) Representative changes in the input/output function of the summating
potential (SP) following inner (IHC) and outer hair cell (OHC) loss. Selective destruction of IHCs reduces the SP amplitude particularly for
low- to mid-intensity sounds. Additional loss of OHCs results in a further reduction in SP amplitude particularly at high intensities.
20
type I afferent nerve fibers with carboplatin also greatly
reduces the SP (Durrant et al., 1998). Although the inner
hair cells are believed to make a dominant contribution
to the SP, additional loss of outer hair cells further
reduces the amplitude of the SP.
1.5.3.3. Compound action potential
The compound action potential (CAP) is the result of
the synchronous firing of spiral ganglion neurons
of the auditory nerve in response to sound stimulation.
Thus, the CAP represents an extracellular potential
which can be measured in or near the cochlea.
The CAP consists of two negative peaks, the first
(N1) occurring with a latency of approximately
1 ms, and the second (N2) occurring with a latency
of roughly 2 ms following the presentation of
moderate- to high-intensity sound stimuli (Figs. 16D
and 18A). Both the amplitude and latency of the
CAP peaks are dependent on the intensity of the sound
stimulus. The amplitude of the CAP response
increases with increasing stimulus intensity, while
the latency of the CAP peaks decreases with increas-
ing stimulus intensity (Fig. 18B). The CAP threshold,
N2
N1
B OHC Loss
80
70
Stimulus Level (dB)
60
50
40
30
20
10
0
0 1 2 3 4 5
Time (ms)
Fig. 18. (A) The compound action potential (CAP) consists of two major negative peaks (N1 and N2). (B) The CAP amplitude increases while
N1 and N2 latencies decrease with increasing stimulus intensities. (C) Representative changes in the input/output function of the CAP fol-
lowing selective inner (IHC) or outer hair cell (OHC) loss. Selective IHC loss reduces CAP amplitude at mid- to high-intensity levels with little
effect on CAP threshold, while selective OHC loss only slightly reduces the CAP amplitude but causes a large shift in the CAP threshold.
S.H. HAYES ET AL.
the lowest stimulus intensity required to evoke a
reliable CAP response, is typically 10–20 dB
above an individual’s behavioral hearing threshold
(Eggermont and Odenthal, 1974). Because of this,
the CAP is commonly used clinically as a measure
of hearing sensitivity.
Similar to what is seen with the CM and SP, selec-
tive inner or outer hair cell loss has predictable effects
on the CAP (Fig. 18C). Selective loss of inner hair
cells results in a reduction in the amplitude of the
CAP with only a modest change in the CAP threshold
(Wang et al., 1997). In contrast, selective outer hair
cell loss causes a shift in the CAP threshold with only
a small reduction in amplitude once the threshold is
exceeded at high intensities (Özdamar and Dallos,
1976). The CAP provides information about the func-
tional integrity of the auditory nerve. For example, the
number of auditory nerve fibers contributing to the
CAP can be inferred from the amplitude of the peaks,
while the width of the CAP can be used as a measure of
the synchrony of auditory nerve firing. The CAP is
also used clinically to distinguish between SNHL
and conductive hearing loss (CHL). A reduction in
C
800 Control
700 IHC Loss
600
CAP Amplitude (uV)
500
400
300
200
100
0
0 20 40 60 80 100
dB SPL
ANATOMY AND PHYSIOLOGY OF THE HUMAN AUDITORY SYSTEM
the CAP amplitude with normal peak latencies is
characteristic of SNHL which is commonly a result
of damage to or a reduction in the number of auditory
nerve fibers. Conversely, individuals with a CHL
require a higher intensity stimulus to elicit a CAP
but the slope of the CAP amplitude is not greatly
affected.
1.6. Conclusion
This chapter provides the reader with an introduction
to how the external, middle and inner ear transform
environmental sounds into an organized pattern of
neural activity that is transmitted to the central audi-
tory system where it can be perceived. With a basic
understanding of the auditory periphery, clinicians
and scientists can better appreciate the functional basis
of hearing deficits and their underlying mechanisms.
Although the fundamental characteristics of the exter-
nal, middle and inner ear have been revealed by the
pioneering work reviewed herein, it is likely that future
studies which employ advanced techniques (e.g.,
genetic manipulation and high-resolution imaging) in
laboratory animal models will continue to add to our
understanding of the precise workings and dysfunction
of the mammalian peripheral auditory system.
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