The document provides an overview of the inner ear anatomy and physiology. It describes the cochlea as a snail-shaped bony structure that is coiled around a central axis. Within the cochlea lies the membranous labyrinth, which contains three fluid-filled scalae separated by membranes. Sound causes vibrations that move fluids and stimulate hair cells in the organ of Corti. Inner hair cells detect sound and transmit signals, while outer hair cells amplify these signals. Key structures that enable hearing include the stria vascularis, which generates the endocochlear potential providing energy, and potassium circulation pathways that are essential for normal cochlear function.

1. Auditory Physiology : Inner Ear
Dr. Diptiman Baliarsingh
1st Year PG, Dept. of ENT,
Hi-Tech Medical College & Hospital,
Bhubaneswar

2. Introduction
 Snail-shaped osseous structure
 Coiled 2 & 2/3 turns around a central axis –
Modiolus
 With in the bony cochlea (osseous labyrinth) lies
the membranous labyrinth, consisting of –
 Central scala media – cochlear duct
 Superiorly, Scala vestibuli separated by Reissner’s
membrane
 Inferiorly, Scala tympani separated by basilar
membrane
 The connection of scala vestibuli with the middle
ear occurs at Oval window, which is attached to

3. Cross-section of Cochlea

4.  The Round window links the scala tympani to
the middle ear & is covered by Round window
membrane
 The scala vestibuli & scala tympani merge at the
apex of cochlea – Helicotrema, & scala media
ends blindly
 S.V. & S.T. are filled with perilymph, extracellular
fluid with High Na+ & Low K+
 S.M. is filled with endolymph, composed of High
K+ & Low Na+
 Cochlear Endolymph has electrical potential of
+85mV
 This difference in ion composition and electrical
potential difference provide energy for cochlea’s

5.  Functional units of cochlea
 The Organ of Corti – sensor of cochlea, converts &
amplifies mechanical sound to electrical signals
(Mechano-electrical Transduction)
 Stria Vascularis – cochlea’s battery, generates
energy (Endocochlear potential)
 The Spiral Ganglion – these are neurons featuring
axons, electrical wires, transporting signals from
cochlea to CNS.

6. The Organ of Corti & surr. structures

7. THE ORGAN OF CORTI
 Named after – Alfonso Giacomo Gaspare Corti
 It consists of two types of sensory receptors –
inner and outer hair cells
 There are about 3500 flask shaped Inner Hair
Cells, lined up in a single row, through out entire
length of S.M.
 Lateral to IHC’s lies 3 rows of Outer Hair Cells,
cylindrical shaped.
 They contain hair bundles consists of Actin-filled
stereocilia, graded acc. to height, with the most
lateral being the tallest and most medial row
being the shortest.

8.  The hair bundles of IHC’s are organized as a
smooth curved line of 2-3 rows of stereocilia &
OHC’s stereocilia bundles are arranged in a
shallow V-shape.
 They are Mechano-sensitive organelles of H.C.’s
 Every H.C. sits over a phalangeal supporting cell,
i.e. Deiters Cells for OHC’s
 The inner and outer pillar cells delienate the area
between IHC’s & OHC’s framing the Tunnel of
Corti
 Other supporting cells embrace the hair cell-bearing
part of organ of corti

9. Cochlear Stereocilia

10.  Medially, Inner Marginal Cells
 Laterally, Hensen’s (Outer Marginal) Cells
 Clauduis Cells
 Boettcher Cells
 The O.o.C. is covered by Tectorial membrane
along its entire length, an acellular structure and
is medially attached to spiral limbus & connects
hair bundles to OHC’s.

12. The BASILAR MEMBRANE &
TONOTOPY
• Sound  eardrum  vibration  ear ossicles 
inner ear
• Movement of stapes causes displacement of
cochlear fluid in scala vestibuli
• The incompressibility of perilymph causes a
pressure gradient between SV & ST, leading to
movement of Basilar membrane & Organ of Corti
• Its like a TRAVELLING WAVE moving from base
to apex along the basilar memb.

16.  A pure tone stimulus, the travelling wave moves
from base to apex, reaches a Maximum* at a
characteristic place along basilar memb. and
then decays
 This precise location of this Maximum depends
on Frequency of stimulus – the principle of
tonotopic organisation of cochlea
 The base is tuned for frequencies of 20 kHz and
apex for 20 Hz
 The tonotopic gradient is a continuous gradient in
basilar membrane width and also with changes in
hair cell height and length of cellular structures
i.e. stereocilliary hair bundles

17. Tonotopic organization of Organ of Corti

18. Inner Hair Cells &
Mechanoelectrical Transduction
 The IHC’s are sensory cells which convert
mechanical stimulation to electrical signals and
the synaptic activity is transmitted to brain
 This M-E Transduction occurs at tips of
stereocilia
 This apparatus is present in all hiar cells &
consists of mechanically gated ion channels,
that is closely asso. with elastic structures & a
Tip-link, that connects the tip of the stereocilium
to the side of the next tallest stereocillium

19.  Components of Stereocilia
 Cadherin 23 & Protocadherin 15 – components of
Tip-Link
 Mechano-Electrical Transduction channel
 Insertional Plaque
 Myosin 1C
 Actin filaments
 Mechanical deflection of hair cell bundles leads
to mechanical tension leading to conformational
change in transduction channel protein &
increase in channel opening
 USHER SYNDROME - Congenital Hearing Loss
+ Progressive loss of vision due to Retinitis
Pigmentosa

21.  On mechanical stimulation
 Towards the TALLEST row of stereocillia – K+ &
Ca++ ions enter hair cell through open M-E T
channels, located near the tips – leads to
DEPOLARISATION of cell
 Towards the SHORTEST stereocillia, the M-E T
channels close – leads to HYPERPOLARISAITON
of cell
 After a sustained excitatory deflection of hair
bundle, the initial large transduction current
ADAPTS, manifesting as decline of current –
correlated with closure of transduction channels
 2 distinct process involved in adaptation
1. Rapid reclosure of transduction channels
2. Sliding of myosin based motor asso. with
transduction appa.

22. Mechanoelectrical Transduction

23.  1st - Rapid Channel reclosure “Fast Adaptation”
 Ca++ binding to intracellular site near ch. gate
 2nd - “Slow Adaptation”
 10 tmies slower than Fast Adap.
 Upper tip-link slides down the stereocilum
 During sustained stimulus, adaptation leads to
resetting of restore point, hence allowing the
transduction apparatus to function at point of
highest sensitivity
 The influx of Ca++ through open transduction
channels leads to slippage of myosin based
adaptation motor, which continuously strives to
crawl towards the stereocilliary tip along actin
core

24.  The slippage of the myosin based motor
channels reduces the tension in the tip-link
complex & lowers the open probability of the
transduction channels, shutting off the Ca++
influx
 At Low Ca++ levels  myosins of the adaptation
motor will effectively move upwards 
readjusting the tension in the tip-link complex to
a point
where the open probability of
the M-E T ch. is close to the
open probability at rest.
 Myosin 1C is crucial for this
adaptation process

25. OUTER HAIR CELLS & AMPLIFICATION
 OHC’s have a key role in amplification of Basilar
memb. motion
 Amplification is necessary for detection of sounds
at low pressure levels
 OHC’s are mainly responsible for
AMPLIFICATION & SHARP TUNING of Auditory
system
 Mechanism of Amplification –
Somatic Electromotility  the OHC’s change
their length by 3-5% in response to electrical
stimulation

26.  When Depolarized, they Contract & when
Hyperpolarized they Elongate
 The OHC’s exert mechanical force causing
movements of basilar memb. motion caused by the
travelling wave
 Prestin – motor protein responsible for somatic
electromotility in outer hair cells. It belongs to SLC26
anion transporter superfamily – mediate
electroneutral exchange of chloride & carbonate
across plasma membrane
 Hypothesis* - intracellular anions act as voltage
sensors which bind to prestin and trigger
confirmational changes
 Hyperpolarisation  anion binding to prestin 
increase in surface area of prestin  cell elongation
 Depolarisation  dissociation of anion  decrease in
the prestin surf area  cell contraction
 At rest  anions are usually bound to prestin  longer

27. TECTORIAL MEMBRANE
 It is an extracellular structure overlying IHC’s &
OHC’s & it changes its size from base to apex
 Only the tallest stereocillia of OHC’s are directly
embeded into the undersurface of tectorial
membrane
 TM is attached on its inner edge to spiral limbus
& is loosely connected to the supporting cells –
Hensen’s cells by trabeculae
 *Mutations in TM genes – Alpha & Beta Tectorin –
caused profound hearing loss
 It is more like a resonant gel which is involved in
enhancing the frequency selectivity of cochlea

28. STRIA VASCULARIS
 Plays an important role in cochlear hemostasis
by generating endocochlear potential &
maintaining the unique ion compostion of
endolymph
 Highly vascularized, multi-layered tissue & is a
part of lateral wall of SM
 3 distinct cell types
 Marginal
 Intermediate
 Basal

29. Stria Vascularis & K+ Circulation

30.  Tight junction demarcate strial tissue & provide
ionic barriers with marginal cells at one end &
basal cells at other end
 The extracellular space between these two
barriers is known as intrastrial compartment
 Marginal cells separate endolymph filled scala
media from interstitial compartment that is filled
with interstitial fluid
 Basal cells separate interstitial cells from
perilymph that surrounds fibrocytes of the spiral
ligament
 The intermediate cells as well as blood vessels
are embeded in intrastrial compartment

31. Passage of ions from Perilymph to Endolymph in SV

32.  Gap junctions connect basal cells with with
intermediate cells & with fibrocytes of spiral
ligament – allowing Electric coupling &
exchange of ions and small molecules
 The regulation of cochlear fluid homeostasis
also involves endolymphatic sac, which
responds to endolymph volume disturbance
 Malfunctions in cochlear fluid homeostasis due
to disruptions of endocochlear potential, ionic
composition, or its volume regulating
mechanism leads to varios forms of hearing
impariment

33. ENDOCOCHLEAR POTENTIAL
& POTASSIUM HOMEOSTASIS
 Hair cell mechanoelectrical transduction works
efficiently due to large driving force for cations to
enter cell’s cytoplasm from scala media
 The +85 mV endocochlear potential of
endolymph & chemical gradient of K+ are the
main components of the driving force
 HEARING THRESHOLD INCREASES
APPROXIMATELY BY 1dB PER 1mV LOSS OF
ENDOCOCHLEAR POTENTIAL

34.  K+ is the main cation of endolymph which
generates endocochlear potential
 Movement of K+ in cochlea –
1. K+ can enter hair cells through
mechanoelectrical transduction channels & is
released through hair cells’ basolateral
membranes into perilymphatic extracellular
space
2. K+ can enter supporting cells and move towards
the spiral ligament by extensive gap junction
network
3. Alternatively, K+ can diffuse extracellularly via
perilymphatic space
 Spiral ligament composed of Type II & Type I
fibrocytes take up K+ and provide an
intracellular pathway into basal & intermediate
cells of stria vascularis

35. K+ flow through the Organ of Corti &
Stria Vascularis

36.  K+ is released by intermediate cells via KCNJ10
channels into interstitial space from which it is
actively pumped & cotransported into marginal
cells
 The marginal cells release K+ into SM
 The K+ circulation is NOT a TRUE
RECYCLING*
 Malfunctions of several K+ channels leads to
perturbation of cochlear K+ homeostasis,
resulting in hearing impairment
For Ex – loss of KCNE1 & KCNQ1 gene
(encodes K+ ch subunits that allow secretion of
K+ from marginal cells to SM) leads to Jervell
and Lange-Nielsen Syndrome chatz by Hearing
Loss & Cardiac Arrhythmia

37. Passage of ions from Perilymph to Endolymph in SV

38.  The most well known genes involved in cochlear
homeostasis are the ones that encode
CONNEXIN Proteins
 Connexins form subunits of gap junction
channels, which underlie K+ circulation networks
described for supporting supporting cells of the
Organ of Corti, the spiral ligament & stria
vascularis
 Mutations involving Connexins 26, 30, 31 & 43
are responsible for majority of non-syndromic
hereditary hearing loss

39. GENE PROTEIN PR. LOCATION PR. FUNCTION DISEASE
KCNE1 KCNE1 Marginal Cells K+ Ch Jervell/Lange-
Nielsen Synd.
KCNQ1 KCNQ1 Marginal Cells K+ Ch Jervell/Lange-
Nielsen Synd.
KCNQ4 KCNQ4 OHC’s & IHC’s K+ Ch DFNA2
GJB2 Cx26 Fibrocy. in SL & SLi
Epi. on BM, I & B Cl
Gap Junction Protein DFNB1/DFNA3
GJB6 Cx30 Fibrocy. in SL & SLi
Supp Cells of OoC
Gap Junction Protein DFNA3
GJB3 Cx31 Fibrocy. in SL & SLi
Epithelia on BM
Gap Junction Protein DFNA2, AR –
nonsynd. deaf
GJB1 Cx32 Fibrocy. in SL & SLi
Epithelia on BM
Gap Junction Protein X-linked Charcot
Marie-Tooth &
Deafness
GJA1 Cx43 Fibrocy. in SL & SLi
Epi. on BM, I & B Cl
Gap Junction Protein AR – nonsynd.
deafness
BSND Barttin Marginal Cells Cl- Ch Ty 4 Bartter’s
Syndrome

40. COCHLEAR FLUID
HOMEOSTASIS
 Perilymph, Endolymph & Interstitial Fluid are 3
types of fluids found in the cochlea & its
metabolic support system
 The proper ionic composition of these fluids is
essential for generation of endocochlear potential
 Perilymph & Interstitial fluid have High Na+ & Low
K+
 Endolymph have Low Na+ & High K+ , Low Ca++

41. Ionic composition of Endolymph & Perilymph
Ions PERILYMPH ENDOLYMPH
Na+ 148 1.3
K+ 4.2 157
Ca+ 1.3 0.023
Cl- 119 132
HCO3- 21 31
pH 7.3 7.5

42.  In stria vascularis , influx of Na+ accompanies
K+ from the interstitial compartment into
marginal cells
 Cotransporter NKCC1 uses strong Na+ gradient
to bring Na+, K+ & 2Cl- ions into marginal cells
 Na+/K+ ATPase sets up this gradient by by
pumping Na+ into intrastrial space in exchange
for K+
 Lastly, K+ leaves marginal cells to enter
endolymphatic space
 This process maintains a High Na+ & Low K+
concerntration of intrastrial fluid, which facilitates
K+ replenishment into intrastrial space

43.  Cl- is transported back to intrastrial space by
CIC-K/Barttin Channels
 Inhibition of NKCC1 & Na+/K+ ATPase by Loop
Diuretic Furosemide & Ouabain leads to
supression of E-C Potential
 Mut. of Barttin gene or Mut. of both CIC-Ka &
CIC-Kb subunits of basolateral Cl- Ch. leads to
Bartter’s Synd Ty 4 chatz by Deafness & Renal
salt wasting
 Na+ is reabsorbed from endolymph by outer
sulcus & Reissner’s Memb cells, which play a
role in maintaining Low Na+ conc of SM

44.  Ca++ regulation – the tip-links break at very low
Ca++ conc. & the mechanoelectical transduction
channels are blocked at high Ca++
concerntrations
 Ca++ carries part of transduction current & plays
critical roles in Adaptation & Cochlear
Amplification
 Ca++ permeable channels – Ca++ ATPases &
Na+/K+ exchangers are also found & regulate
Ca++ efflux & influx into Endolymph

45. Cochlear Fluid Volume
Regulation
 It is equally important for cochlear funtion
 Previously, 2 popular theories – Longitudinal &
Radial Flow patterns
1. Longitudinal Flow of endolymph is the secretion
along the membranous labyrinth with
reabsorption in the endolymphatic duct & sac
2. Radial Flow is based on local secretion &
reabsorption, via stria vascularis
 Today, the prevailing thought is that there is no
significant volume flow under physiological
conditions

46.  A low volume flow inside the cochlea has
consequences for intracochlear drug application,
where under physiological conditions, diffusion
of compounds inside the fluid filled compartment
appears to limit the equal dosing of potential
drugs from base to apex
 At cellular level, transmembranous water
movement depends on aquaporins
 Aquaporin 2 found in Endolymph lining epithelium
of endolymphatic sac & is regulated by
Vasopressin
 Vasopressin also increases the activity of
epithelial Na+ ch & NKCC1 cotransporters found
in strial marginal cells & type II fibrocytes of
spiral ligament

47.  Glucocorticoids have opposite effects – supress
symptoms of Meniere’s disease, by decreasing
vasopressin production & altering expression of
certain aquaporins
 Cochlear fluid homeostasis, Ion transport &
Endocochlear potential are all req. for proper
cochlear function
 Ageing, affects long-term maintainance of
endocochlear potential & lowered metabolic
rates of stria vascularis plays a role in age rel.
hearing loss

48. THE SPIRAL GANGLION
 Located in Rosenthal’s canal within the Modiolus of
the cochlea
 It contains cell bodies of afferent neurons, its
dendrites are excited by neurotransmitter released
by Organ of Corti, hair cells & the axons of which
are projects centrally into the cochlear nucleus, in
brain stem.
 Majority (95%) of afferent fibers are thick &
myelinated, & originate from type I ganglion
neurons, exclusively innervate IHC’s
 Remaining (5%) of afferent fibers are thin,
unmyelinated & originate from type II ganglion
neurons, innervate OHC’s

49. Spiral ganglion innervations

50.  A dozen of type I ganglion neurons innervate
each IHC’s – Converging innervation pattern
 The type II afferent nerve fibers divide into
multiple branches & contact multiple OHC’s –
Diverging innervation pattern
 All auditory information is carried to brainstem
by afferent system, the auditory & vestibular
nerves join each other forming vestibulocochlear
nerve
 Efferent fibers originate in brain stem from
neurons located in Superior Olivary complex &
send information to cochlea by synapsing with
OHC’s & with the afferent fibers beneath IHC’s

51. NEURAL PROCESSING OF AUDITORY
INFORMATION & I.H.C. SYNAPSES
 Afferent NT release by IHC’s is initiated at their 5-30
ribbon type synapses, where local influx of Ca++
through voltage gated Ca++ channels leads to
fusion of synaptic vesicles at presynaptic sites
 Each ribbon synapse is composed of presynaptic
dense body & is surrounded by vesicles containing
NT’s, thick plasma memb, synaptic cleft & post
synaptic region containing AMPA-type glutaminergic
receptors of afferent nuerons

52.  The tonotopic organisation of the organ of corti
is also maintained within the afferent system,
where the depolarisation of IHC’s at specific
location leads to excitation of connected afferent
spiral ganglion neurons
 Each afferent is characterized by a specific
turning curve, that decribes the sound pressure
level of stimulus needed to elicit a response at a
given frequency
 The feature of turning curve is that they show
the frequency at which the nerve fibers displays
highest sensitivity – its characteristic frequency
 Loss of cochlear amplification, i.e. by OHC’s
loss, leads to broadening of turning curve &
increase in fibers’ response thresholds

53.  Tonotopic organisation of cochlea is the basis
for frequency coding in auditory nerve fibres –
Place Coding
 Frequency is coded by auditory nerve fibres’
discharge characteristics – Phase Locking, it
happens only at low frequencies
 Tonotopic organisation & Phase Locking are
both important for frequency discrimination
 Discharge rates are determined by frequency &
intensity of stimulus

54.  As intensity increases, the discharge rate with in
a single auditory nerve fibre increases, & the no.
of auditory nerve fibers activated at a given
characteristic frequency increases with
intensifying stimuli
 The recruitment of more fibers is because of
auditory nerve fibers of same characteristic
frequency have different response thresholds
 With increased stimulus intensity, other afferent
nerve fibres of nearby characteristic frequency
are also activated.

55. EFFERNET INNERVATION OF
COCHLEA
 2 different types of efferent fibers originate in
brain stem
1. Myelinated Medial Olivocochlear (MOC)
Efferents – arise from neurons located around
Medial Superior Olivary Nucleus. They project to
C/L & I/L cochlea, where they form cholinergic
synapses with OHC’s
2. Unmyelinated Lateral Olivocochlear (LOC)
Efferents – arise from Lateral Superior Olivary
Nucleus. Fibers project predominantly into I/L
cochlea, where they terminate on dendrites of
Afferent type I neurons beneath IHC’s
 LOC efferent synapses are neurochemically

56.  The MOC system
 Stimulation of MOC system leads to increased
thresholds, due to decrease in the degree of
cochlear amplification by OHC’s
 This sound-evoked feedback, decreases
sensitivity of hearing apparatus when
metabolically expensive amplifications systems
are not needed
 The LOC system
 Their direct input on afferent neurons, suggests
they regulate afferent activity – affects dynamic
range
 LOC feedback systems are slow & req. minutes to
become effective
 It also additionally functions to perform slow
integration & adjustment of binaural inputs needed
for accurate binaural function & sound localization

57.  The activity of MOC & LOC efferent systems
seems to have protective effects against
acoustic injury, important in loud noise
environments.

58. Thank You...
REFERENCES
 Surgery of the Ear – Glasscock-Shambaugh - 6th
Ed.
 Scott Brown’s Otorhinolaryngology & Head and
Neck Surgery - 7th Ed.
 Cumming’s Otolaryngology & Head and Neck
Surgery - 5th Ed.
 Mohan Bansal – 2nd Ed.