COCHLEAR
PHYSIOLOGY
Introduction..........................................................................
3
History of Cochlear
Microphonics...................................
6
Cochlear
Mechanics..............................................................8
Cochlear Macro mechanics.................................................
10
Traditional
Theories........................................................... 13
Travelling Wave
Theory.................................................... 15
Non – linearity of
cochlea..................................................22
Helicotrema and Rejection
of very L.F’s.......................... 24
Changes
to passive wave in an active cochlea................ 24
Cochlear
Micromechanics..................................................26
Hair
Cell Mechanics............................................................29
Organ of
Corti.......................................................................32
Tactorial
Membrane............................................................ 35
Hair
Cell Responses.............................................................39
Inner
Hair Cells & Receptor potentials..................................40
Input-Output
Functions of I.H.C............................................49
Outer
Hair Cells & Receptor Potentials..................................47
Cochlear
Potentials................................................................54
Receptor
Potentials................................................................57
Cochlear
Microphonic..........................................................57
Summating
Potentials...........................................................61
Compound
Action Potentials.................................................64
Journal
Articles.......................................................................66
Reference...............................................................................67
INTRODUCTION
The
auditory system is one of the specialized sensory systems. The physiological
responses that occur in the cochlea are the foundation of the process of
hearing. Humans can hear sounds with frequencies ranging from 20 – 20000 Hz.
Mammalian auditory systems can also process great sensitivity and respond to
sounds over an intensity range of 120 decibels. Such striking performance is
largely determined by mechanical and biophysical process in the cochlea. The
main task of the human cochlea is to analyze sound in terms of its intensity,
timing and frequency content. To achieve this, sound in air is matched
acoustically to the denser water medium within the cochlea by middle ear,
efficiently producing pressure fluctuations in the cochlear fluids and
vibration of the ribbon like basilar membrane (BM) and the sensory organ of Corti
(OC) perched upon it.
The vibrations of the cochlear
partition (BM) normally take the form of waves or ripple that travel away from
stapes and towards the cochlear apex. This basilar membrane vibrations produce
motion of hair cell stereocilia, which gates stereociliar transduction channels
leading to the generation of hair cell receptor potentials and the excitation
of afferent auditory nerve fibres. At the base of the cochlea, BM motion
exhibits a C.F specific and level dependent compressive nonlinearity. Thus
responses to low level, near CF stimuli are sensitive and sharply frequency
tuned and responses to intense stimuli are insensitive and poorly tuned. This
mechanism involves forces generated by the outer hair cells and controlled,
directly or indirectly, by their transduction currents. At the apex of the
cochlea, nonlinearities appear to be less prominent than at the base, perhaps
implying that the cochlear amplifier plays a lesser role in determining apical
mechanism responses to sound. Whether at the base or the apex, the properties
of basilar membrane vibration adequately account for most frequency specific
properties of the responses to sound of auditory nerve fibres.
Thus cochlea can be considered as a transducer
that converts the vibratory stimulus into a form usable by the nervous system.
The Cochlea ;
·
Separates stimulus
frequency into different spatial regions of the auditory system.
·
Converts changes in
pressure into vibrations in the discharge of auditory neurons and from the
original acoustic signal the temporal confirmation is perceived to a remarkable
extent.
Two breakthroughs lead to a
re-assessment of cochlear physiology. The first was the discovery of
otoacoustic emissions, which provided strong evidence for the existence of an
active, energy-generating process in the cochlea. The second was the discovery
by Brownell (1983) of outer hair motility, which provided a potential physical
substrate for the active process.
Propagation
of Sound within the cochlea
One point of view is that the
movements of the stapes are transmitted directly to the fluid column in the
cochlea which responds as a whole- a mass action mechanism. As in below figure,
inward movement of the stapes footplate causes the perilymph to flow up the
scala vestibuli, through the helicotrema, and then down the scala tympani,
where the round window are distended by an amount directly proportional to the
inward movement of the stapes. During outward movement, the direction of flow
of the fluid column is reversed. Sound energy, transmitted to the vibrating
fluid column, is selectively absorbed by the structures on the basilar
membrane.
Mass-action through the cochlea. Inward
movement of the stapes footplate causes perilymph to flow up scala vestibuli,
through the helicotrema, and down scala tympani, where the round window is
distended.
Another view point is that the
pressure generated in the scala vestibuli is transmitted across the scala media
to the scala tympani. As shown in figure (2), such a transmission of pressure
results in distortion of vestibular membrane and, in turn, the basilar
membrane. As before, however, there will be displacements of round window that
are out of phase with the direction of movement of the stapes. The fluid
movements may be distinctive for a particular frequency and thus produce
distortion of the basilar membrane at a specific frequency-related locus. In
either of these mechanisms, disturbances of the hair cells located on the
basilar membrane transform the mechanical energy into electrical disturbances
that stimulate the fibres of the cochlear nerve.
Schematic representation of the path of
vibrations through the cochlea. Vibrations are transmitted across the scala
media, into scala tympani.
Brief History of Cochlear Mechanics
·
1561: Gabriello
Fallopio discovers the snail-shaped cochlea of the inner ear.
·
In 1760 Cotigno
announced that cochlea is filled with fluid and with air.
·
In 1851 Alfonse Corti
described the structures of the sensory organ, now named after him. But the
function of each component was unclear.
·
In 1863 Hensen first
recorded steriociliary bundle on sensory receptor cells. He suggested that the
steriocilia play an important role in the excitation of these cells
·
In 1863 HelmHoltz
proposed that analysis of sound and mechanism of hearing through Fourier
analysis, which was hypothesized in 1943 by Ohm. He reasoned that our frequency
discrimination must be due to the vibration of a series of independent
resonators within cochlea.
·
1928 - Georg von Bèkèsy
begins to use large-scale models of the cochlea to determine precisely how
sounds of different frequencies stimulate the organ of Corti.
·
1930 - In the 1930s, G. E. Wever and C.W. Bray discover
that auditory nerves discharge in synchrony with sound frequency.
·
1957 - Eberhardt
Zwicker, Smith Stanley Stevens, and Gordon Flottorp show that the auditory
system functions as if divided into 24 critical channels
- In 1960’s the first measurements of the vibrational response to sound of the BM were carried out by George Von Bekesy, for which he was awarded the 1961 Nobel Prize for physiology or medicine, Working principally in the ears of human cadavers, Bekesy showed that
a.
The cochlea performs a
kind of spatial fourier analysis , mapping frequencies upon longitudinal
position along the basilar membrane.
b.
He described a
displacement wave that travels on the basilar membrane from base to apex of the
cochlea at speeds much slower than that of sound in water. As it propagates,
the travelling wave grows in amplitude, reaches a maximum and then decays. The
location of the maximum is a function of stimulus frequency: High frequency
vibrations reach a peak near the base of the cochlea, whereas low frequency
waves travel all the way to the cochlear apex.
c.
Vibration didn’t occur
as a single resonance of the independent resonator.
d.
Cochlear non linearity
or distortion phenomena
·
1966 - Heinrich
Spoendlin discovers that up to 95 percent of auditory nerve fibres terminate on
the inner hair cells.
·
In 1972 Dallos and co
workers reported that OHC are necessary for normal cochlear sensitivity and
neural sensitivity and thresholds are elevated when OHCs are selectively
destroyed.
·
In 1975 Ryan and Dallos
and in 1978 Dallos and Harris proposed direct interaction between OHCs and IHCs
provide a frequency dependent sensitizing influence to IHCs.
·
Kemp in 1978 observed
that a brief acoustic click elicited an echo from cochlea that couldn’t be
explained by the simple linear vibration.
·
In 1980 Dallos reported
origins of prominent non linear processes found in OHC.
·
1989: Patuzzi, Yates,
and Johnstone found that most cochlear disruptions known to reduce neural
sensitivity also reduce OHC receptor current, and that the mathematical
relationships between the drop in receptor current and the (resultant)
threshold elevation are quantitatively very similar for most cochlear
disruptions.
COCHLEAR MECHANICS
The general function of the
cochlea is to translate the mechanical vibration of the stapes and the inner
ear fluids into neural responses in the auditory branch of the VIIIth cranial
nerve. The auditory nerve interacts with the hair cells by way of synaptic
junctions, and hair cells are attached to the basilar membrane by the
supporting cells. Thus, the vibration of the fluids causes the basilar membrane
to vibrate, which in turn causes the cilia of the hair cells to bend. The
bending of the cilia causes the hair cells to start the initiation of a neural
potential, which is sent along the auditory nerve. Thus the hair cells, in
connection with the basilar membrane, translate (transducer) mechanical
information into neural information (the inner hair cells are the actual
biological transducers), that initiate a complex series of events, ultimately
leading to the perception of sound.
The
function of the cochlea.
In general cochlear mechanics may be defined as the phenomenon which
deals with the dynamic responses of the cochlea during acoustic stimulation and
the ways in which the mechanical events are believed to set the stage for
transduction into the electromechanical events that stimulates fibres of the
cochlear nerve.
The cochlear mechanics
can be described in 2 classes
- Micromechanics
- Macro mechanics (BM mechanics)
The vibration of BM and Organ of
Corti relative to the surrounding bony structures is known as macro mechanical
vibration, while the complex vibration of parts of the O.C relative to one
another is known as micromechanical vibration. Both these vibrations are
normally atomic or at most molecular vibrations, comparable with the width of a
cell membrane (less than 10 mm), and they are not independent : not only does macro
mechanical vibration of the BM “drive” the macro mechanical vibration of the
OC, but the micromechanics greatly affect the macro mechanics.
For a pure tone stimulus, the wave
grows as it travels, reaching a maximum at a position known as the wave’s
characteristic place, and then collapse abruptly so that no vibration exists
beyond a cochlear position known as the wave’s cut off region. The characteristic place and cut off region
are positioned along the cochlear length according to the place- frequency map:
high frequencies towards the cochlear base, closer to the stapes and low
frequencies closer to the cochlear apex.
COCHLEAR
MACROMECHANICS
MOTION
OF THE COCHLEAR PARTITION
·
The structure of the
cochlea can be simplified considerably; it can be treated functionally as if
the cochlea were uncoiled and the whole cochlear partition were a single
membrane separating scala vestibule from scala tympani.
·
Furthermore, in terms
of how sound energy ultimately is utilized by the cochlea, it is the properties
of the basilar membrane which are of greatest importance, to the extent that it
is generally equated with the cochlear partition in the simplified cochlea.
·
As the stapes is pushed
inward, a difference in pressure, or pressure
gradient, develops across the cochlear partition. Since the fluids of the
cochlea are incompressible, something has to give, so the basilar membrane is
deflected towards the scala tympani. The displaced fluid, in turn, causes the
outward displacement of the round window. As the stapes moves outward, the
opposite happens. The basilar membrane is deflected upward and the round window
is pulled inward. Thus, as the stapes vibrates in the oval window, the basilar
membrane, indeed the entire contents of the cochlear partition, is set into an
up and down motion following the alternating motion which follows the
alternating pressure gradient across it. Thus, most of the vibratory energy
delivered by the stapes to the cochlear fluids is coupled to the basilar
membrane.
·
Although the middle ear
provides the most efficient route of communication, the basilar membrane can
also be set into motion by vibrating the skull.
·
For any given frequency
of sound impinging upon the ear, the up-down displacement of the basilar
membrane will vary in amplitude along its length; however, except for the most
intense and/or very low frequency sounds, the whole membrane will not be set in
motion simultaneously.
·
The peak-to-peak
amplitude gradually increases until a certain distance is reached, after which,
there is a rapid reduction in the displacement.
·
All possible
instantaneous values of displacements are contained within a pattern or what
might be called the envelope.
·
Examining the motion
along the whole length of the basilar membrane (for one frequency), a wave is
observed to move from the base to apex. This is called a travelling wave. It always progresses from one end of the cochlea
to the other, specifically from base to apex.
·
Along the basilar
membrane the waves are never stationary, as would be the case if a string
vibrated at a modal frequency. That is why the waves in the cochlea are called “travelling waves”.
·
The waves start slowly
as they move onto the shore, build up to a peak, and then break off
dramatically.
·
One of the constraints
in the cochlea, is the limited width of the medium (the basilar membrane), so
the travelling wave envelope can be seen as a bulge in the membrane.
·
CHARACTERISTICS
OF THE WAVELENGTH
·
The wavelength is
constantly changing with distance, becoming shorter as the wave approaches the
apex.
·
This, in turn, leads to
a progressively increasing time lag of the motion of the basilar membrane (in
reference to the motion of the stapes), due to the increasing arrival time of
the wave.
·
These factors suggest
that the medium of the wave, the basilar membrane, must have properties
changing with distance. Its width varies from the base to the apex which
suggests variations in stiffness and mass.
·
It also seems likely
that different frequencies will optimally activate different regions of the
basilar membrane, since these factors are expected to have frequency-dependent
effects on the motion of the membrane.
·
It was the late Nobel
laureate Georg Von Bekesy who first demonstrated travelling waves in the
cochlea and to whom the travelling wave theory is attributed.
·
In cadaver specimens of
human cochlea, he observed that, indeed, low frequency sounds elicit travelling
waves which have their maxima near the apex and as the frequency increases the
maximum of displacement moves towards the base.
·
It is the location at which the peak of the
envelope occurs which is believed to be the basis for the brain’s decision as
to the pitch of a sound.
·
In effect, the cochlea
performs a spectrum analysis of the sound entering the ear wherein it
translates the frequency(s) of the sound into distance(s) along the basilar
membrane – a frequency-to-place
or tonotopical transformation.
·
Each frequency
contained in a sound creates its own travelling wave. For complex sounds such
as speech, the resulting pattern of vibration along the cochlear partition is
also quite complex since the component travelling waves are all superimposed.
·
The primary determinant
of the frequency-to-place transformation is, specifically, the stiffness of the
basilar membrane. The variation in its width from base to apex brings about an
approximate 100:1 change in stiffness, wherein it is most stiff in the base,
where it is narrowest, and least stiff in the apex, where it is widest.
·
The friction and mass
of the structures resting on the membrane and of the basilar membrane itself
cannot be ignored.
·
The viscosity of the
fluids surrounding the basilar membrane and its own internal friction determine
the damping in the motion of the travelling wave.
·
The gradient of stiffness along the basilar
membrane is the key factor determining the tonotopical transformation. It is
important to note that the elasticity of the membrane itself (per unit area)
does not change significantly along its length.
TRADITIONAL THEORIES
1.
RESONANCE PLACE THEORY
·
Given by Helmholtz
(1895).
·
He proposed that the
basilar membrane was constructed of segments that resonated in response to
different frequencies, and that these segments were arranged according to
location (place) along the length of the basilar membrane.
·
To achieve this tuning,
the segments at different locations would have to be under different degrees of
tensions.
·
A sound entering the
cochlea causes the vibration of the segments that are tuned to (resonate at)
the frequencies that it contains. Because the resonators are laid out according
to place, the locations of the vibrating segments signal along which
frequencies are represented.
·
2.
TEMPORAL (or FREQUENCY) THEORIES
·
Rutherford’s “Telephone
Theory” claimed that the entire cochlea responds as a whole to all frequencies
instead of being activated on a place-by-place basis.
·
All aspects of stimulus
waveform would be transmitted to the auditory nerve (like a telephone receiver
connected to the telephone wire), and then the frequency analysis is
accomplished at higher levels in the auditory system.
3. VOLLEY PRINCIPLE
·
Given by Wever (1949).
·
He proposed that
several neurons operating as a group could fire in response to each cycle of a
high-frequency sound, even though none of them can do so individually.
·
This is possible if one
neuron fires in response to the next cycle (while the first nerve cell is still
in its refractory period), etc.
4. PLACE-VOLLEY THEORY
·
Given by Wever &
Lawrence (1954).
·
It involves the
combined operation of both place and temporal mechanisms. Low frequencies are
handled by temporal coding, high frequencies by place, and an interaction of
the two mechanisms occurs for the wide range of frequencies between the two
extremes.
5. SOUND PATTERN THEORY
·
Given by Edwald, it is
one of the non-resonance theories.
·
According to this
theory, a sinusoidal movement of the stapes sets up a series of standing waves
along the basilar membrane, with wavelengths varying according to frequency.
·
It is the task of the
nervous system to resolve the separate stimuli spread out over the membrane
into the impression of a single tone. A different vibratory pattern or “sound
image” represents a different tone.
·
Because the entire task
of analysis is related to the nervous system, whose activities were completely
unknown, it was not possible to draw any further conclusions on the basis of
this theory.
Travelling
Wave Theory
The cochlea is a complex hydro-mechanical
system activated by the motion of the stapes footplate. Inward motion of the
footplate produces an increase in pressure in the perilymph near the oval
window. Outward motion results in lowered pressure. Because the bony cochlear
capsule is inflexible, an outward or inward bulging of the round window
membrane compensates for the pressure on the cochlea. However, to reach the
round window, the pressure must be absorbed by and transmitted across the
cochlear partition. Because the partition is flexible, it can be displaced in
both directions and transfer the pressure change to the fluid in the region of
the round window. The resulting energy exchange between the surrounding fluids
and the moving partition initiates a characteristic wave pattern that
progresses along the partition from the base to the apex. Because of its
progression along the cochlea, the phenomenon is known as a travelling wave.
The development of the TW along
the BM is dependent on the vibratory input to the cochlea that is provided by
the stapes. In general, compression waves drive the BM downward and the
rarefaction waves drive the BM upward (von Bekesy, 1960, 1970).
RECENT MEASUREMENTS IN T.W-An
Experimental Study
The more recent results regarding
the travelling wave are a development of the approach pioneered by G. von
Bekesy and our current knowledge will be introduced through a discussion of his
work. Von Bekesy in a long series of experiments, described in a collected form
(von Bekesy, 1960), examined the movement of the cochlear partition in human
and animal cadavers. Temporal bones were rapidly dissected soon after death and
were immersed in saline solution. Rubber windows were substituted for the round
and oval windows, and a mechanical vibrator was attached to one of them. The
cochlear wall was opened under water for observation of the partition within.
By microscopic and stroboscopic observation of silver particle scattered on
Reissener’s membrane, von Bekesy was able to plot out the now-classic travelling
wave pattern as shown below.
Fig:5
Travelling waves in the cochlea were first shown by von Bekesy. The full lines
show the pattern of deflection of the cochlear partition at successive
instants, as numbered. The waves are contained within an envelope which is
static (dotted lines). Stimulus frequency: 200Hz.
Von Bekesy presumed that this was
similar to the movement of membrane carrying the transducers themselves, namely
the basilar membrane. For a stimulus of fixed frequency the cochlear partition
vibrated with a wave that gradually grew in amplitude as it moved up the
cochlea from the stapes, reached a maximum, and then rapidly declined. The wave
of displacement moved more and more slowly as it passed up the cochlea, so the
phase changed with distance at an accelerating rate. And the apparent
wavelength of the vibration decreased. However, the frequency of vibration at
any point was, of course, the same as that of the input.
Von Bekesy’s plots were made in
two ways. By opening a length of cochlea it was possible to see the pattern of
movement distribution along the membrane, and so plot the waveforms and their
envelopes for sounds of different frequencies. The vibration envelopes found by
von Bekesy are shown in figure below.They show the important point that as the
frequency of the stimuli was increased, the position of the vibration maximum
moved towards the base of the cochlea. Thus high frequency tones produced a
vibration pattern peaking at the base of the cochlea. Low-frequency tones, in
contrast, produced most vibration at the apex of the cochlea, although, because
of the long tail of the vibration envelope, there was some response near the
base as well.
Fig:6 Displacement envelop on the
cochlear partition are shown for tones of different frequency. The slower plot
shows the relative phase angle of the displacement.
A second way in which von Bekesy measured the vibration pattern is
indicated in the figure below. He opened the cochlea at certain points, and
measured the vibration at those points as the frequency was varied. Figure (7)
shows his results for six points on the membrane, the peak-to-peak stapes
displacement being kept constant as he varied the frequency at each point. Note
that, as before, it is the most basal point that responds best to the highest
frequencies. Note the shallow slope on the low-frequency side, and much steeper
slope on the high-frequency side. In going from the space axis of figure (5) to
the frequency axis of figure (7) the direction of variation of the parameters
marked on the curves and the abscissa have to be reversed, although the
position of the steep and shallow slopes are the same.
Von Bekesy’s results can be
summarized as follows: vibration of stapes give rise to a travelling wave of
displacement on the basilar membrane. For a vibration of a particular frequency,
the vibration on the basilar membrane grows in amplitude as the wave travels
towards the apex, and then, beyond a certain point, dies out rapidly which is called
the cut off region. The wave
travels more and more slowly as it travels up the cochlea. Low-frequency sounds
peak a long way along the membrane, near the apex, and high frequency sounds
only a short way along, near the base. On the basis of his results, therefore,
the basilar membrane appears to act substantially as a low-pass filter.
Figure (7): Frequency responses are
shown for six different points on the cochlear partition.
The amplitude of the travelling wave was envelope was measured as the
stimulus frequency was varied with constant peak stapes displacements. The
position of the point of observation is marked on each curve.
FREQUENCY AND INTENSITY REPRESENTATIONS
IN COCHLEA
The sound wave is a very important
aspect in the analysis of sound by the auditory system, because the pattern of
movement of the basilar membrane depends on the frequency of stimulus. For a
sine wave of a single frequency, the vibration has a sharp peak which is
confined to a narrow region of the basilar membrane. This means that the
mechanical system shows a high degree of frequency selectivity. The frequency
selectivity depends on the mechanics of the basilar membrane and the cochlear
fluids, and their interaction with hair cell responses.
The basilar membrane composed of
fibrous and connective tissue stretches radially from the spiral lamina to the
spiral ligament and longitudinally from the base of the cochlea to the apex.
·
Length of the BM is 32
mm (David J, JASA, 1980).
·
The width of the
basilar membrane increases from about 150 µm in the base to approximately 450µm
in the apex.(Musiek F. & Baran J. 2007).
·
The stiffness of the
basilar membrane decreases from base to apex.
Because of the structural differences of the
partition, the travelling wave does not maintain uniform amplitude throughout
the cochlea. From its origin at the base, it increases in amplitude while
progressing toward the apex until it reaches a maximum, beyond which it
declines rapidly. Moreover, the location along the cochlea at which the
travelling wave reaches its largest amplitude changes with the frequency of the
stimulating signal. High frequency stimuli generate the maximum wave amplitude
at the base of the cochlea. For low frequencies, the maximum amplitude of the
displacement is toward the apex (von Bekesy, 1984).
The physical characteristics of the
BM play a role in the velocity of the TW (Dallos, 1996) the basal end which is stiffer
and smaller is prone to quick movements (i.e. higher frequencies). Zwislocki
(2002) relates that at the basal most aspect of the cochlea, the TW velocity is
100m per second and it slows down to about 2 – 4 m per second at or near the
apex.
Also because of the base-to-apex
changes in width, mass, and, especially, stiffness, the ability of the
partition to absorb energy from high-frequency changes in fluid pressure is
diminished toward the apex. Hence, high-frequency energy excites only the basal
region, whereas low-frequency energy is allowed to travel further along the
cochlea (von Bekesy, 1949, 1960). The end result is that different frequencies
of stimulation produce displacement envelop maxima at different locations along
the cochlea. The vibrations of all but the lowest audible frequencies do not
travel the entire length of the cochlear partition. Instead, they die down
before reaching the helicotrema. High-frequency stimuli are extinguished quite
close to the base, whereas low-frequency stimuli are propagated further toward
the apex (Figure: 8).
Different locations are thus tuned
to different stimulus frequencies. The hydro-mechanical wave action of the
cochlea map the frequency of a given stimuli in the spatial extent and maximum
amplitude of the travelling waves that the stimulus produces. If two
different frequencies are received by the cochlea simultaneously they will each
create maximum displacement at different points along the basilar membrane.
This separation of complex signal into different maximal points of displacement
along the basilar membrane corresponding to the sinusoidal components of which
the complex signal is composed means the B.M is performing a type of spectral
analysis also called as BAND PASS
FILTER ACTION of the B.M.
Figure (4): Diagram of travelling wave
envelopes for three frequencies. Amplitude of displacement greatly exaggerated.
Also there is greater displacement
of the BM for high intensities compared to low intensities. Hence, it can be
concluded that the excursion size of the TW is related to the intensity of the
stimulus and the peak of the excursion is related to the frequency component of
the stimulus.
NON-LINEARITY OF COCHLEA
As the intensity of the acoustic
stimulus increases, the peak displacement of the BM becomes broader and grows
in amplitude, but with considerable compression across the intensity range.
This is especially in the case of high intensities.
Ruggero (1992) made some
comparisons for a 3 dB SPL and an 83 dB SPL 9 kHZ tone in an animal model. If
the basilar membrane responses were linear, the 83 dB SPL tone should have
yielded a BM deflection that was 10,000 times greater than the deflection that
would have occurred for the 3 dB SPL tone. If so the deflections would be so
great that the BM would hit the bony structures of the cochlea during both
negative and positive deflections causing significant trauma to the BM and the
hair cells. But this obviously does not happen. Instead there were major
compression effects that resulted in an amplitude increase of only 4 times over
this intensity range. This compression function within the cochlea serves as a
protective mechanism to the O.C. These measurements were made at high
frequencies. It was observed that there is less compression for low frequencies
than there is for high frequencies (Rhode & Cooper, 1996).
At very low intensities, the BM
gets a boost from the cochlear amplifier resulting in increased BM excursions.
These effects are more greatly seen for high frequencies.
This mechanical amplification of
low intensity tones and the compression of high intensity tones were also
demonstrated by comparing BM responses to those of the stapes (Ruggero,1992 ;
Geisler, 1998). Unlike the BM response, the stapes’ displacement for acoustic
stimulation is close to linear. The BM response to a weak tone (3 dB SPL at 9
kHz) is much greater than that of the stapes and as the tonal intensity
increases, the BM response compresses while the stapes displacement increases
linearly.
The travelling wave progresses from
the base to the apex because of the difference in the physical characteristics
of the basilar membrane, not because the oval window first stimulates the
cochlear base. In fact, the travelling wave has an identical pattern if
stimulation is provided artificially at the cochlear apex. Moreover,
progression does not occur because energy is transmitted from one region of the
basilar membrane to the adjacent region. An incision made entirely through the
basilar membrane does not affect the nature of the travelling wave (von Bekesy,
1960).
THE HELICOTREMA - REJECTION OF VERY LOW
FREQUENCIES
·
Called the helicotrema,
the canal ensures that slow or low-frequency pressure fluctuations introduced
into either the scala vestibuli or the scala tympani are distributed almost
equally to the other chamber, preventing a large differential pressure across
the partition and damaging displacements of hair cells.
·
For such low
frequencies, an oscillatory movement of the stapes simply pumps perilymph
through the helicotrema and displaces the round window.
·
It should be emphasized,
however, that the helicotrema is only effective for very low frequencies: above
a particular cut-off frequency (normally a few hundred Hertz, depending on the
size of the helicotrema and therefore the species; Dallos 1970; Ruggero,
Robles, and Rich 1986a,b), the helicotrema is unable to pass pressure
fluctuations because the combination of the fluid mass and viscosity within its
small cross-sectional area forms an effective ‘acoustic plug’.
Most pressure fluctuations of
audible frequency cannot pass through the helicotrema and do not make it as far
as the helicotrema in any case. Rather, they take a “short cut” through the
cochlear partition near the cut-off region for the stimulus frequency
CHANGES
TO THE PASSIVE WAVE IN AN “ACTIVE” COCHLEA
·
It has been assumed so
far that the macro-mechanical vibration is purely “passive,” or powered solely
by the incoming sound. The passive waves propagating in such a passive system
may or may not travel in the forward or reverse direction (from and to the stapes
respectively), depending on the site of the perturbation along the cochlea and
its frequency relative to the cut-off frequency of each cochlear region
encountered in its travels.
·
Probably the most
important realization in cochlear physiology has been that OHCs inject
mechanical energy into a travelling wave as it passes them, creating a larger
vibration than would be present otherwise.
·
The resulting active wave shares many of the features
of the passive travelling wave, and it grows relative to the passive wave as
long as the active hair cells are adding energy to it. With such active
assistance, a much lower sound level is required to produce particular
amplitude of vibration or a particular hair cell or neural response.
·
In addition, the active
travelling wave is more localized along the cochlear length, apparently due to
the decreased damping or improved “quality factor” for each incremental segment
along the cochlear length, due to the partial cancellation of friction by the
active hair cells.
·
Finally, the active
wave is labile, reverting to the passive travelling wave if the active process
is disrupted or at high sound levels when the active process appears to become
relatively less important.
·
The progressive change
from an active vibration pattern at low sound levels to a passive pattern at
high sound levels is responsible for much of the nonlinearity in cochlear
mechanics.
COCHLEAR MICROMECHANICS
The main areas of interest in
cochlear hair cell mechanics is the tip links and their ability to open and
close ion channels and electro-motility of OHCs.
It’s assumed that
1.
The macro-mechanical
vibration of the BM platform upon which the OC rests is not at all affected by
the complicated micromechanical properties of the OC.
2.
The micromechanical
vibration of each segment of the OC along the cochlear length is independent of
all other segments.
Although neither assumption is
correct, both are useful when introducing the main concepts of cochlear
micromechanics. To a great extent, the focus of cochlear function is to direct
mechanical stimulation to the stereo cilia of the IHCs. Therefore, a reasonably
complete understanding of the mechanics of cochlea must explain how the
vibrations of the cellular and membranous components of the cochlear partition
result in deflections of the IHC stereo cilia. Thus, it’s of immense strength
to investigate the “micromechanics” of the cochlea i.e how various sites of the
organ of corti, the BM, and the TM move in relation to each other, preferably
in individual ears.
COCHLEAR FLUID COMPARTMENTS
Inside the bony labyrinth of the
cochlea is a membraneous cochlea that consists of three fluid filled canals that
spiral around the modiolus. The scala vestibuli is the largest of the canals.
The scala tympani extends from the round window to the apex of the cochlea and
communicates with the cochlea through a small opening called the helicotrema.
The SV and the ST contain perilymph which is similar in composition to CSF
(i.e. high Na+and low K+). Lying between the ST and the
SV is another fluid filled duct known as the scala media. It consists of
endolymph which is similar to intracellular fluid (i.e. high K+ and
low Na+). The ionic composition of endolymph is such that it gives
rise to a positive endocochlear potential that is critical for normal cochlear
functioning.
STEREOCILIA TIPLINKS AND SIDELINKS
Stereocilia which emerge in
rows from the apical surfaces of the IHCs form a gently curving arc. The row of
stereo cilia is arranged in a staircase pattern with the tallest row facing the
lateral wall of the cochlea and the shortest row facing the modiolus. The rows
of stereo cilia on the OHC are arranged in a W pattern; the stereocilia are
graduated in height with the tallest row facing the lateral wall.
The stereocilia maintain a constant
thickness along most of their length but taper to a narrow shaft as they enter
the cuticular plate which creates a point where the stereocilia can pivot when
they are deflected. The cilia are composed of actin which makes them rigid.
Two types of filaments form
lateral cross links within and between the rows of stereocilia which are called
the ‘sidelinks’. The sidelinks
hold the stereocilia together causing the bundle to move in unison when
mechanical force is applied to the bundle. A thin filament called the ‘tiplink’ courses from the shaft
of one stereocilium to the tip of the shorter stereocilium in the next shorter
row. As the stereocilia bundle is deflected in the direction of the tallest row
of stereocilia, tension increases in the tiplink. This in turn pulls open the
mechanically gated ion channels located near the tip of the cilia.
The graded heights of the cilia
set up the function of the tiplinks. The crosslinks support the cilia and allow
the cilia to move in unison. The tiplinks open up pores in the cilia to allow
ion flow through channels whenever the cilia are deflected toward the tallest
cilia (excitatory). These pores and their associated ion channels are closed
when the cilia are deflected in the opposite direction. (Inhibitory).
STRIA VASCULARIS
The stria vascularis plays a
critical role in maintaining the ionic composition of the endolymph and the
endocochlear potential. The electrical potential and the ionic composition of
endolymph is maintained by several different ion transport mechanisms that
recycle potassium from the endolymph through the sensory hair cells, the
fibrocytes in the spiral ligament, the cells of the stria vascularis and back
into the endolymph. When the stereocilia are deflected, K+ in the
endolymph flows through the hair cells into the perilymph, through the spiral
ligament and stria vascularis, and then back into the endolymph. Ions also flow
from the endolymph to the stria vascularis through the outer sulcus cells and
through Reissener’s membrane.
Four ion transport mechanisms have been identified maintaining the high
K+ concentration in the endolymph
·
A selective K+
channel, located on the apical membrane of the marginal cells which releases K+
into the endolymph. The membrane potential across the apical surface of
the marginal cells is about 0 to +10 mV, and the activation and deactivation of
K+ is relatively slow (Marcus et al 1998).
·
The electrogenic Na+/K+
ATPase pump are located in the basolateral membrane of the marginal
cells. During one cycle of ATP hydrolysis, the marginal cells take up 2 K+
ions and three Na+ ions that are extruded into the interstitial fluid.
·
The Na+/2
Cl-/K+ co-transporter
contributes to the uptake of an additional three K+ ions from the intrastrial space as well as Na+ and Cl-
·
Finally a Cl- channel
also located on the basolateral membrane of marginal cells contributes to the
flow of Cl- from the marginal cells into the intrastrial space. As a
result of these mechanisms, the concentration of K+ in the
intrastrial space is quite low while that inside the intermediate cells is
quite high. Although the marginal cells are responsible for the movement of K+
from the intrastrial space to the endolymph, it is the large potential
difference between the intrastrial fluid and the cytosol of the intermediate
cells that is now thought to be responsible for the +80 mV endocochlear
potential. These play an important role in hair cell transduction.
Hair
cell mechanics
Upon stimulation the BM begins to
move in either an upward direction towards the scala vestibuli or a downward
deflection toward the scala tympani depending on the phase of the stapes
movement.
Condensation wave inward
movement of stapes downward deflection of BM (inhibitory)
Rarefaction wave
outward movement of stapes upward
deflection of BM (excitatory).
If the compression wave results in
the BM being deflected downward, it will not result in a hair cell firing until
the rarefaction segment of the wave causes the BM to move upward. On the other
hand, a rarefaction stimulus will result in the hair cells firing immediately.
During a compression wave the OHCs
move away from the limbus as the BM rotates downward. The OHCs cilia which are
attached to the tactorial membrane move towards the limbus because the membrane
is stretched by the deflection of the BM (inhibitory). Although the cilia are
relatively stiff, they rotate quite easily at their bases. In downward
deflection the cilia rotate counter clockwise. Because the stereocilia are
interconnected by side links (Pickles, Comis & Osborne), all the cilia on a
hair cell bend with this shearing force.
Since the IHC’s cilia do not
touch the tactorial membrane their deflection must be indirect. The most likely
scenario is that the fluid in the sub-tactorial is pushed away or toward the
IHC’s cilia. This could be a result of the deflection of the OHCs’ cilia
pushing fluid toward the IHCs when there is downward movement of the BM. It is
possible that the Hensen’s stripe, an eminence protruding downward from the
underside of the tactorial membrane immediately above the IHCs, may play a role
in the deflection of the IHCs stereocilia. More specifically, as the fluid
flows in the sub-tactorial space to the region of the IHC cilia, Hensens’s
stripe may cause a constriction, adding to the force of the fluid flow against
the cilia. The cilia of the hair cells are arranged in rows of different
heights.
During a compression stimulus,
the cilia are bent toward the limbus. This results in the tiplinks losing their
tension on the so called trap door and the trap door closes entirely -hyperpolarisation.
Conversely when there is a rarefaction
stimulus the cilia are pushed toward their tallest neighbour which causes
considerable tension on the tiplinks and the trapdoor is opened to allow ion
flow into the cells -depolarisation.
It has been stated that movements of 100 nm are sufficient to open the ion
channels.
Q. What happens to the
cochlear hair cells when a particular region of the cochlear partition is set
into motion?
The effective stimulus to the
cochlear hair cells causes the displacement of their stereocilia from their
resting position (Hudspeth & Corey, 1977; Richardson & Cody, 1986). In
some of earlier theories of hearing, the up-and-down movement of hair cells and
contact of the stereocilia with the tactorial membrane were thought to be the
active stimulus for the neural impulse of hearing. For the outer hair cells,
the displacement is thought to occur as follows. The hinge points about which
the basilar and tactorial membranes rotate during the displacement of the
cochlear partition are different. Also outer edge of the tactorial membrane is
not firmly attached to the organ of Corti. The effect of this arrangement is
shown below picture. Vertical displacement of the cochlear partition drags the tactorial
membrane across the surface of the organ of Corti and produces a radial
shearing force on the longest row of the outer hair cell- sensory hairs
(Dallos, 1992) whose tips are embedded in tactorial membrane (Kimura).
Probable pattern of
shearing action between the tactorial membrane and the organ of Corti. The
hairs of inner hair cells, which are not attached to the tactorial membrane,
are thought to be displaced by fluid movement. Bottom: Organ at rest. Top:
during displacement toward scala vestibuli. From Ryan & Dallos (1996)
Organ of
Corti
The organ of Corti rests upon the
basilar membrane; it is obvious that the travelling waves produce certain kinds
of mechanical movements on it. The structure of this organ favours mechanical
deformation of the inner and outer hair cells and the stereo cilia that project
from their upper surfaces. The effect of the basilar membrane displacement on
the hair cells depends upon structures that surround these cells, such as the
arches of Corti and the tactorial membrane.
Arches of Corti
The motion of the arches of
Corti during propagation of a travelling wave is rather complex. Let’s consider
the basilar membrane as a ribbon with its ends fixed. In below figure an instantaneous
wave form of the basilar membrane is shown. Displacement along the longitudinal
axis is less along p than along q because the former is closer to the boundary
of the lateral suspension at the spiral lamina.
Schematic drawing of an instantaneous waveform
of the basilar membrane in longitudinal and traverse cross sections
Fig:21 (a) Longitudinal motion of the vertex of an
arch of Corti at locus y. (b) Vertical and radial motions of the vertex
of an arch of Corti at locus y.
The resultant displacement
of the vertex toward the apex is through angle
.Recall that at an instant one-half cycle later, the membrane
would have a displacement in the form of a mirror image, so that the vertex
would then be displaced toward the base.
The Dieters’’ cells with their phalangeal
processes, the reticular lamina, the cells for lateral buttressing, and the
fluid (or fluids) of the scala media all place constraints upon movement. Nevertheless,
the inner and outer hair cells, inclined as they are along the inner and outer
pillars, clearly are subject to mechanical deformation by movements of the more
rigid arches of Corti.
The mechanical couplings of the
structure of the organ of Corti make the arches especially well suited to the
conversion of longitudinal travelling waves on the basilar membrane to radial
shearing forces as shown below.
However, downward movement of the
pillar results in a shear toward the outer hair cells (OHC), whereas upward
movement results in a shear toward the inner hair cells (IHC). Whereas downward
movement of the outer pillar has a strong effect, upward movement shows little
effect, and such effect as occurs passes through an inflection.
Figure (20): The effects of displacement
of the outer pillar of an arch of Corti, measured in arbitrary angular units,
on radial movement (solid line) and vertical movement (dashed line) of the
arch’s vertex, measured in arbitrary linear units. The solid line should be
read against the left ordinate, the dashed line against the right ordinate.
Tactorial
membrane
As shown above, the tactorial membrane has its
fulcrum at or near its medial attachment to the limbus, tactorial membrane is
thinnest. It, too, undergoes motion during propagation of a travelling wave,
and it is believed to play an important role in cochlear mechanics through its
intimacy with the stereocilia of the hair cells. Many of the stereocilia of the
outer hair cells actually penetrate the gelatinous underside of the tactorial
membrane.
Part (a) of figure (21) represents
the mechanical means by which the tactorial membrane is supposed to deform the
stereocilia of the outer hair cells. In the middle panel of part (a) the tactorial
and the basilar membrane are identified, along with their respective places of
pivot. The shaded rectangle represents an outer hair cell with a cilium arising
from its top and embedded in the tactorial membrane at radius r. Radius r
represents the locus of the centre of the base of the inner hair cell. Because
of the difference in location of the fulcra (shown as open circles), upward and
downward movements produced by travelling waves deflect the stereocilia to and
fro along the radial axis. Whereas upward movement bends the stereocilia toward
the stria vascularis, downward movement bends them in the opposite direction,
toward the modiolus.
The nature of coupling within
the organ of Corti no doubt leads to some bending of stereocilia along the
longitudinal axis. However, the stereocilia probably do not bend very much in
the longitudinal direction because of the rather firm support from the
surrounding structures. Clearly, the arches of Corti provide primarily for
radial shear. Vertical forces may change the shape of the hair cell itself,
causing it to become first fatter and then thinner with downward and upward
movement, respectively.
Part (b) of figure (21) shows the
interaction between the radial shearing produced by the tactorial membrane and
that produced by the arch of Corti. The downward displacement of the basilar
membrane, and therefore of the outer pillar, produces a radial shear toward the
stria vascularis, a direction exactly opposite to that produced by the tactorial
membrane. The consequence is that the stereocilia are bent to a greater extent
than would be the case if either shear operated alone.
Figure (21): (a) A schematic
representation of the way the movements of the tactorial and basilar membranes
bend the stereocilia of an outer hair cell. (b) The interaction of opposing
shear forces from the tactorial membrane (solid arrow) and the arch of Corti
(open arrow). On the upper right is the displacement of the stereocilia.
Due primarily to the 100-fold change in the
stiffness of the basilar membrane, compressional sound waves in cochlear fluids
produce membrane patterns that have maximum displacements at different places
along the membrane as a function of sound frequency; and the precision with
which the places are defined by mechanical means is adequate to account for the
frequency tuning of the first order acoustic nerve fibres’. Further, the
gradient of stiffness produces places according to a log frequency scale,
with the low tones at the apex and the high tones at the base. Phase lags
result in a travelling wave that moves the organ of Corti in such a way as to
convert the longitudinal wave into two opposing radial shear forces, one
produced by the arches of Corti and one produced by the tactorial membrane,
that mechanically deform the hair cells and their stereocilia.
It is clearly established that
sensory hair cells transduce mechanical into electrochemical activity when
their stereocilia are bent. Specifically, sensory hair cells like those in
cochlea are activated when their stereocilia are bent in a particular direction
and inhibition occurs when they are bent in opposite direction. This concept is
shown in figure (22). Bending of the stereocilia toward the basal body
(centriole or rudimentary kinocilium) results in excitation, while bending in
the opposite direction (away from rudimentary kinocilium) is inhibitory.
However, the basal body found at the base of the “W” shaped arrangement of
stereocilia on the OHC’s. The base of the “W” faced toward the outside of the
cochlear duct (away from the modiolus). Therefore, the process of cochlear hair
cell activation involves the bending of the stereocilia away from the modiolus.
Figure (22):
Directional sensitivity of sensory hair cells.
The travelling waves result in
longitudinal motion of the basilar membrane (rod of Corti) and radial motion of
the tactorial membrane, which in turn shear the cilia of the hair cells so that
they bend outward (away from the modiolus) when the membrane are deflected
upward (toward scala vestibuli), resulting in depolarization of the hair cell.
The stereocilia of the outer
hair cells (OHCs) are in intimate contact with the overlying tactorial membrane
(except for the shorter ones); whereas the preponderance of information
suggests that the inner hair cell (IHC) cilia do not make such contact. These
differences imply alternative means of communicating the movements of the
membranes to the stereocilia of the two types of hair cells. Subsequent studies
have confirmed that the IHCs are activated by the velocity of basilar membrane
movement. In other words, the OHCs respond to the amount of displacement and
IHCs respond to the rate at which the displacement changes.
The reason for this difference
in the mode of activation is consistent with the different relationships of the
inner and outer hair cell cilia to the tactorial membrane. Since the OHC cilia
attach to the tactorial membrane, an effective stimulus is provided by the
relative movement of the reticular and tactorial membranes, which depend upon
basilar membrane displacement. The IHC, on the other hand, stand free of the tactorial
membrane. Their stimulus is thus provided by the drag imposed by the
surrounding viscous fluid as the basilar membrane is displaced; the greater the
velocity of the basilar membrane displacement, the greater the drag exerted
upon the cilia.
Hair Cell Responses
The
measurement of the hair cell responses was one of the important recent
landmarks in the progress of the cochlear physiology. Inner hair cells of the
mammalian cochlea were first recorded from by Russell and Sellick (1978). Since
the very great majority of afferent auditory nerve fibres’ make their synaptic
contacts with inner hair cells, it must be presumed that it is the job of inner
hair cells to signal the movements of the cochlear partition to the central
nervous system. Hair cell responses will be dealt with in terms of the resistance-
modulation and battery theory of Davis (1958), In this theory, the endocochlear
potential and the negative hair cell intracellular resting potential combine to
form a potential gradient across the apical membrane of the hair cell.
Movement of the cochlear partition produces deflection of the stereocilia. The
deflection opens ion channels in the stereocilia. Ions are driven into the cell
by the potential gradient, causing intracellular voltage fluctuations.
Intracellular depolarization causes release of transmitter, activating the
auditory nerve.
Inner Hair Cells
The
membrane of the inner hair cell, like all cell membranes, is semi-permeable,
which means that certain ion can penetrate the cell membrane while others rejected.
An ion pump maintains a steady- state balance of ions across the membrane such
that the interior of the cell is negative relative to the environment that
surrounds it. Russell and Sellick (1978) recorded intracellularly from inner
hair cells of the mammalian cochlea. They found resting potential of some – 45
mV. The inner hair cell is sensitive to displacements of its stereocilia along
a single radial axis, and depending upon the direction of displacement, the
effect on the cell membrane is to depolarize (excitatory) or to hyperpolarize
(inhibitory).
The movement of the stereocilia toward the
stria vascularis is believed to open up channels, located in their tips,
through which passes K+ ions drawn down the stereocilia by the negativity
inside the hair cell. An influx of K+ ions serves to depolarize the hair cell
membrane in a wave that spread quickly to the base of the hair cell. At the
base of the hair cells there are believed to be calcium channels in the hair
cell membrane. Their opening and closing are voltage dependent. During
depolarization the calcium channels open, and calcium ions also enter the hair
cell at its base. In ways not fully understood, calcium ions appear to cause
the pre-synaptic vesicles to fuse with the hair cell membrane and then release
their contents into the synaptic space between the hair cell membrane and
dendrites of the afferent neurons.
Thus
depolarization leads to the production of action potential in the auditory
nerve. Movement of the stereocilia away from the stria vascularis closes the
channels to potassium ions and leads to hyper-polarization of the hair cells.
Hyperpolarization of the cell membrane closes the calcium channels and thus the
initiation of neural spike activity in the postsynaptic cells.
I.H.C RECEPTOR POTENTIAL
Figure (30): Intracellular voltage changes in an inner hair
cell for different frequencies of stimulation show that the relative size of
the AC component declines at higher stimulus frequencies (number on right of
the curves).
It is
possible conceptually to divide the potential changes in the hair cells into an
AC response at the stimulus frequency, and a sustained DC depolarization.
At the
basal turn of the cochlea, an IHC for 300 Hz tone burst produces a
predominantly AC response that depolarises and hyperpolarises around the
resting potential. The AC response to low frequency tones is asymmetrical, with
the depolarizing phase being significantly larger than the hyperpolarizing phase.
The asymmetry results in an AC
response that rides upon a DC depolarization. As the stimulus frequency is
raised, the AC component of the voltage declines relative to the DC component,
so that frequencies of a few kHz and above, the AC component are much smaller
than the DC component [lower traces, figure (30)]. Russell and Sellick (1983)
described this to the capacitance of the hair cell membrane. Hair cell
membranes, like all cell membrane have capacitance and capacitance offer low
impedance to AC currents at high frequencies. At high frequencies, therefore,
the AC current was short circuited by the low impedance of the hair cell
membrane, reducing the AC voltage response of the cell.
At the
apical turn of the cochlea the IHC show maximum responses around the CF and the
responses drop off rapidly at frequencies above and below CF at moderate
intensities.
I.H.C Relation
to the Basilar Membrane Response.
The close correspondence between
hair cell responses and basilar membrane responses can be shown in several
ways. First, the tuning curve for an inner hair cell is shown in figure (31).
The curve has a low threshold, sharply- tuned tip, at the best or
“characteristic” frequency (CF). There is also a high threshold and broadly-
tuned tail, stretching to low frequencies. The shape corresponds to the tuning
curve for the mechanical response of the basilar membrane .The tuning of inner
hair cells therefore appears to be derived from the tuning of the basilar
membrane, although it is possible that there are some differences in the high
threshold tail.
Figure
(31): Inner (o) and outer () hair cells have very similar tuning curves. The
curves are also very similar to those for the mechanical response of the
basilar membrane
Correspondingly, intensity
functions for inner hair cells are similar to those of the basilar membrane
mechanical response [figure (32); Around
the CF (17 kHz) for this particular hair cell), the response grew linearly at
first, at the rate of a 10- fold voltage change for a 20 dB increase in
stimulus intensity, parallel to the dotted line. When the intensity was raised
further, the response at and near CF grew nonlinearly, i.e. with a shallow
slope. At frequencies above CF the response saturated to a low maximum output
voltage, and well below the CF (e.g. 2 kHz) the response grew entirely
linearly. Again, both of these indicate that inner hair cell responses closely
follow basilar membrane mechanical response.
Figure (32): AC intensity functions for
an inner hair cell show an approximately linear increase in potential at the
lowest intensities at each frequency, followed by saturation. The parameter
marked on each curve shows the frequency of stimulation in kHz; this cell was
most sensitive at 17 kHz. Dotted line: slope for linear growth.
Input – output
functions of I.H.C
The relations between the acoustic
stimulus and the responses can be described by the input –output function.
Here, the instantaneous value of the input stimulus pressure is plotted against
the instantaneous value of the intracellular potential [figure (33)]. It is
possible to construct these functions only for low – frequency stimuli, where
the AC component of the intracellular response has not been attenuated by the
capacitance of the cell walls. The function is asymmetric in various ways.
First, the maximum excursion in the
positive, depolarizing direction is greater than the maximum excursion in the
negative, hyperpolarizing direction. Secondly, the maximum depolarization is
reached much more gradually and at much greater sound pressure excursions, than
the maximum hyperpolarization. The function in figure (33) describes how in
response to sinusoidal stimulation, the depolarizing potential changes in the
hair cell are greater than the hyperpolarizing ones.
Figure (33): Input – output functions
are made by plotting the instantaneous value of the intracellular voltage
change (vertical axis) against the instantaneous value of the stimulus pressure
during sinusoidal stimulation (horizontal axis). The function for an inner hair
cell shows voltage changes in the depolarizing direction (upwards) that are
greater than those in the hyperpolarizing direction (downwards). Stimulus
frequency: 600 Hz
Outer Hair Cells
Outer hair
cells have proved to be particularly difficult to record from. One reason may
be that outer hair cells are suspended by their apical and basal ends within
the space of Nuel, so that an advancing electrode tends to push them aside
rather than penetrate. The position of outer hair cells halfway across the
cochlear duct, rather than the edge, may also mean that they can move more
easily away from the electrode. Davis proposed that the two resting potentials
(endocochlear (+80 mV) and intracellular (-70 mV) create a steady resting
current flow across the organ of Corti through the hair cells. The outer hair
cells are mechanically distorted by radial shearing forces produced by the
relative movement of the reticular lamina and the tactorial membrane, between
which lies the stereocilia. Movement of the stereocilia may displace the
cuticular plate, which, in turn, changes the electrical resistance at the top
of the hair cell, where stereocilia penetrate the hair cells. Modulation of
resistance controls the release of neurotransmitter into the hair cell-
dendrite synapse.
O.H.C RECEPTOR POTENTIALS
AC and DC
responses can be recorded from the OHCs but they tend to be smaller than in
IHCs. Both the IHCs and OHCs produce an AC response to low frequency tone but
the OHC response is smaller and predominantly hyperpolarising whereas the IHC
response is depolarising. The characteristics of the OHC’s AC responses are
level dependent. AC responses are symmetrical at low levels, predominantly
hyperpolarising at moderate levels and depolarizing at high levels. OHCs and
IHCs produce little or no AC response to high frequencies but the IHCs produce
a large DC depolarization response whereas the OHCs produce only a small
depolarization.
Dallos and
his colleagues recorded in the apical (low- frequency) end of the guinea-pig
cochlea (Dallos et al, 1982; Dallos, 1985, 1986). With stimulation at moderate
intensities at the CF, they showed that there was a depolarizing DC response
superimposed on the AC component. Unlike the basal turn OHCs, the DC component
could become hyperpolarizing at frequencies just below CF. Figure (35) shows
how the DC component changed polarity with stimulus frequency. If the stimulus
intensity was raised, the frequency range over which depolarization could be
obtained spread, so that the response became consistently depolarizing.
Figure (35): AC and DC responses of an
outer hair cell at the apical (low- frequency end of the guinea-pig cochlea.
The hair cell shows a DC depolarization for stimuli near the best frequency
(800 Hz), and DC hyperpolarization for stimuli 500Hz. The stimulus intensity
was kept constant at 30 dB SPL.
The hyperpolarizing DC component
seen with low-frequency, medium- intensity, stimuli in outer hair cells can be
explained by an input- output function in which the excursions in the
hyperpolarizing direction are larger than those in the depolarizing direction.
Unlike the other DC components which appeared and disappeared instantaneously
with the AC response, the high-intensity DC component in basal turn outer hair
cells took several cycle to develop, and several cycles to disappear after the
end of the stimulus. This suggests that it cannot simply been thought of as a
distortion component of an AC response, and that a description in terms of an
input-output function is not appropriate. Here, the DC response might, for
instance, be metabolic, or due to factors such as changes in the ionic
environment of hair cell produced as result of the acoustic stimulation.
Figure (36):
Input- output for an outer hair cell in the base of guinea-pig cochlea.
The lack of DC component in
basal turn outer hair cell, at moderate and low intensities of stimulation by
high frequency sinusoids has an interesting implication. Since the AC current
will be shunted through the capacitance of the cell wall, the intracellular AC
voltage change can be expected to be small at high frequencies. This suggests
that if to check outer hair cell function in hearing, it is the AC current
through the outer hair cell that is most likely to be important.
O.H.C Relation
to Basilar Membrane Responses
Figure (34): Intensity functions for an
outer hair cell are similar to those of inner hair cells, although the response
saturates more abruptly at high intensities.
Motility
of O.H.C
Motility of
variety forms can be demonstrated in hair cells. Ashmore (1987) showed that
outer hair cells isolated from guinea-pig cochlea were unable to change length
in response to current introduced through an electrode. The cells shortened
when the cell was depolarized and elongated when the cell was hyperpolarized.
Analogous motility has been found by Brownell et al. (1985) and Kachar et al.
(1986)
OHC has distinctly different motile
responses. They are:
A.
Fast motility:
OHC motility that occurs within the same time domain as that of input acoustic
vibration travelling through the cochlea. These would be length changes
occurring within an exponential time course having latency at 120 microseconds.
The electro motility is fast & occurs at frequencies up to the level of
human hearing. The fast contraction can be triggered by mechanical displacement
of stereo cilia (Evans & Dollos, 1993)
Studies of isolated hair cells have demonstrated that the electro motility is
elicited by changes in voltage across the OHC membrane (Santos & Sachii,
1991) and appears to be produced by different molecular motors along the length
of the cell. Thus, fast motility is voltage dependant and not due to ionic
current (Asmore, 1987). The molecular motors are embedded in the cell membrane
of OHC. This was shown by preservation of electro motility. Even when
intra cellular proteins are digested, shortening and lengthening of the OHCs is
about 5 %.
B.
Slow motility:
Stimulation of hair cells and also result in a second form of electro-motility,
gradual changes in length that occur over the course of seconds (Ohnishi, Hara,
Inoue, et al. 1992).
A
slower motile process, with a time-constant of several seconds, was shown by
Zenner et al. (1985), also in outer hair cell isolated from the guinea-pig
cochlea. Changing the
concentration produced a slow contraction or extension
of the cell body. In other experiments, contraction could be produced by the
application of ATP or inositol triphosphatase to the cell (Zenner, 1986;
Schacht and Zenner, 1987).
In these experiments, contraction was
accompanied by the tilting of the cuticular plate. This can also be elicited by
pharmacological agents including acetylcholine which has inhibitory affect on
OHC motility. It’s released by efferent nerve endings terminating on the OHC.
Slow motility may be due to interaction of actin & myosin, osmotic changes
within the cell.
The mechanisms of the various
forms of motility are unclear. Motility of first type is not affected by
changes in the
or ATP concentration, nor by application of the anti-actin
or anti-tubulin drugs (Ashmore, 1987; Holley and Ashmore, 1988). These findings
together with the speed of the response, suggests that the motility is produced
by a direct physical mechanism, rather than processes such as actin-myosin
interactions. Suggested mechanisms involve the movement of charged components
of the cell in the electric field (Kachar et al. 1986). Holley and Ashmore
(1988) found that the motility persisted in cells which had been artificially
swollen into a spherical shape by direct pressure injection, and suggested that
the mechanism of motility resided in structures closely connected to the plasma
membrane. Certain specializations are known here, since outer hair cells have
numerous cisternae lining their lateral walls, connected to the outer membrane
by a regular arrangement of pillars (Flock, 1986).
The
slower motility of the second type could possibly involve actin-myosin
interactions of the sort seen in muscle cells, perhaps involving the actin
filaments which circle the cuticular plate or those which descend from the
cuticular plate through the cell body. There also evidence for other processes
involving structural changes in the cytoskeleton, such as the polymerization of
actin filaments (Zenner, 1986). Slow motility also results from osmotic changes
within the cell or changes in the subsurface cisternae (Dieler, Shehata-Dieler
& Brownell, 1991).
The Role of OHC Motility in the
Organ of Corti
The
discovery of active mechanical responses has revolutionized our understanding
of cochlear mechanics and the transduction process. How the mechanical response
of the individual outer hair cell interact with the motion of the cochlear
partition is not yet clear. Brownell et al. (1985) and Ashmore (1987) suggested
that length changes in the outer hair cells would lead to a dimensional change
in the organ of Corti. An upward movement of the basilar membrane moves the
stereocilia in the excitatory direction, and so produces intracellular
depolarization. Intracellular depolarization shortens the hair cells,
flattening the organ of Corti. It was suggested that this would serve to
enhance the upward movement of the basilar membrane (Ashmore, 1987). However,
the outer hair cells are interconnected by the cytoarchitecture of the organ of
Corti and thus if many these cells move in synchrony their mechanical response
sum up. Since the tallest stereocilia are embedded in the tactorial membrane,
they can influence the motion of that structure as well.
Measurements
of the force generated by individual outer hair cell indicate that the
activation of large numbers of cells in concert should be able to change the
mechanical responses of the cochlear partition (Iwasa and Chadwick, 1992). One
result of this is thought to be amplification of the basilar membrane motion in
a narrow frequency range. That is, the outer hair cells are thought to be the cochlear
amplifier. This interpretation consistent with the loss of
threshold sensitivity and tuning that is observed in the cochlea after outer
hair cell loss (Dallos & Wang, 1974; Harrison & Evans, 1979; Ryan &
Dallos, 1975).
The slower
forms of motility are unlikely to be involved in the amplification of the travelling
wave; they are too slow to feed back on a cycle-by-cycle basis. However, it is
quite possible that they are involved in adjusting the mechanical state of
cochlea over a long term, keeping it in the optimal mechanical state to detect
auditory stimuli.
Electro-motility
characteristics of OHC implicate that the outer hair cells themselves can
induce basilar membrane motion, which has important implications for the origin
and significance of the oto-acoustic emissions.
Cochlear
Potentials
Electrical activity is an integral
part of the functioning of cells in the cochlea & central auditory system.
Cochlear potentials are electrical events produced within the cochlea due to
complex series of electrophysiological events. They also help in the
transformation of mechanical acoustic wave into neural activity.
Cochlear potentials
Resting potentials
Receptor Potentials/
Stimulus evoked
Endocochlear
potentials
Microphonics
(CM)
Intracellular potentials Summating
potentials (SM)
&
Compound Action
Potential (CAP)
Ø Resting potentials
: They are the potentials which occur in the absence of acoustic stimulation
& include potentials of IHCs & other hair cells.
Ø Stimulus – evoked
potentials : They are the potentials that occur in
response to acoustic stimulation. They arise when the activity of a group of
cells (become react entertained) to a specific stimulus, resulting in synchronous
electrical activity.
The second way of classifying
electrical potentials in according to the type of electrode that is used to
record and consequently, the size of cellular population that contributes to
the response.
Ø Cellular Potentials:
Includes the membrane and intracellular potentials, of IHCs & OHCs &
action potentials of individual AN fibres that are recorded using fine tipped,
high impedance metal electrodes or glass micropipettes. These potentials
provided detailed information regarding the behaviour of individual cells
Ø Local Field Potentials:
Reflecting the extracellular electrical activity arising from groups of cells
are recorded by means of low impedance (less than 100 Kohm) electrodes that are
inserted directly into the cochlea auditory nerve. The contribution of any
given cell to the total LFP will depend on its proximity to the recording
electrode & size of its extracellular field potential. LFP’s are typically
quantified in terms of amplitude (total voltage) & provide information
regarding the behaviours of aggregates of cells.
Ø Gross Potentials:
Generated by large populations of cells & are recorded with relatively
large low impedance electrodes, including trans-tympanic electrodes. Gross
potentials such as the CAP can be used clinically to evaluate the functioning
of the auditory periphery. Other potentials measured from the cochlea can
provide insight into how the various elements & various structures of cochlea
function in normal and improved ears.
Ø Resting
Potentials
I. Endocochlear Potential:
Endolymph is among very few extracellular fluids to be very high in K+ &
the proper ionic balance of the cochlear fluids has a profound effect upon the
function of organ of corti.
Bekesy (1952) first explored the
electrical properties of the fluid spaces of the cochlea by recording changes
in electrical potential as an electrode was advanced through the cochlea of a
guinea pig.The endocochlear potential is a ‘+ve’ DC potential of about 80 mv.
It can be recorded from endolymph. It’s assumed to be produced by the energy
consuming, ion pumping process in the stria vascularis.
Source
: The EP was originally thought to be a
diffusion potential resulting from differences in ion concentration between
endolymph and perilymph. However studies have shown that decreasing the k+
concentration gradient between endolymph & perilymph by injecting potassium
chloride into the perilymph has little effect on amplitude of the EP. (Konishi
& Kelesey, 1968). Thus the source of the EP isn’t simply the concentration
gradient between the scala media & the peri-lymphatic spaces.
Several lines of evidence indicate
that the Stria Vascularis is the source of endolymph & the EP & that
generation of the EP is an active energy consuming process. These are as
follows
1.
The EP decreases
significantly when the stria is damaged surgically or with ototoxic drugs
(Davis et al 1958,)
2.
Na+/k+ ATPase activity
is very high in stria vascularis (Kujipers &Bonting 1970). Ouabin, a drug
that inhibits Na+/ka+ ATPase activity, decreases the concentration of K+ &
increases the concentration of Na+ in the scala media & reduces the EP
(Konishi et al, 1978)
3.
‘+ve’ electrical
potential can be recorded from the marginal cells of the stria vascularis even
after Reissner’s membrane is destroyed ( Tasaki & Spyropoulos,1959)
4.
EP declines rapidly
during anoxia (Johnston & Sellick 1972)
These results indicate that the
EP is a metabolic potential, generated by energy consuming activities of cells
in the stria vascularis.
II.Intracellular
Potentials
Tasaki et al (1954) confirmed the negative
resting potential in the organ of corti, with magnitude of about -60 to -10 mv.
This was called as intracellular potential.
Source:
The origin of this potential has been the subject of some controversy. It was
concluded that it’s an intracellular potential due to following reasons:
1)
This potential can’t be
recorded for more than a few minutes, which suggest that it’s due to an
individual cell which stops functioning after a while because of the damage
caused by the invading electrode. The potential would be recordable for longer
duration if it were extracellular.
2)
If cortilymph had a
negative potential, there could be no polarization difference between the
insides of the hair cells & the auditory nerve fibres & their
surrounding fluid, because the functioning of these cells depends upon the
presence of polarization differences across their membrane.
The net result of the ‘+ve’ EP &
the ‘-ve’ intracellular potential is an electrical polarity difference as much
as 160 mV or more across the reticular membrane.
Receptor
Potentials:
1.
Cochlear
Microphonics
It’s an AC receptor potential
that occurs due to the presentation of the acoustic stimulus. It is a potential
similar to the one produced by microphone & exactly reproduces the
waveform. The original recording of the CM were made by Wever & Bray
(1930),who observed that the cochlea acts like a microphone transducing sound
into analogue change, in voltage. If voltage are amplified & fed to a
loudspeaker, the original stimulus will be reproduced with remarkable fidelity.
Adrian (1931) coined the term cochlear microphonic to describe it.
ü Generation
of CM:
It’s generated in the OHC in the
basal part of BM. Bekesy (1950) demonstrated that CM’s are elicited by BM
reflection. Tasaki et al (1954) provided the first evidence that hair cells are
the source of CM. They measure the CM while advancing a recording electrode
through the cochlea. The CM grew in amplitude as the electrode neared the
reticular lamina, and then reversed polarity as the electrode entered the scala
media. These results indicated that CM was generated by hair cells or some
other structure close to the reticular lamina. Studies have shown that large,
sharply tuned CM potential can be recorded from electrode close to the hair
cells (Goodman et al, 1982)
Zheng et al (1997a) conducted experiments with
chinchillas that have selective basal IHC lesions associated with sectioning
the AN showing that basal IHC loss has no appreciable effect on the CM recorded
from the RW. Takeno et al (1994), Trantwein et al (1996) used a unique animal
model in which the IHCs are selectively destroyed by Carboplatin while OHCs
remain intact providing further evidence that IHCs make little, if any
contribution to the CM, collectively these results suggest that the CM is
predominantly generated by the OHCs.
ü Recording
Of Cochlear Microphonics:
The
method of generating CM consisted of placing 1 electrode in the scala tympani
& one in the scala vestibule- one on each side of BM. These electrodes are
then connected to a differential amplifier which records the difference
potentials between the 2 electrodes.
Recording of CM using this method
may be affected by CM potentials generated in the adjacent turns of cochlea.
Therefore, the other methods such as micropipette in the scala media or 2
electrodes placed close to each other in the same scala are used.
ü Generation
of CM:
There are several theories, but Davis’s
variable resistance model has enjoyed the widest acceptance. Think of the
source of the cochlear resting potentials as biological batteries, generating a
current flowing through the scala media, the basilar membrane and the scala
tympani. A sound stimulus would then be represented electrically (the CM) if it
caused the resistance to current flow to change in accordance with the stimulus
wave form.
In other words, the movements of cilia
modulate the resistance, which in turn sets up an alternating current. This AC
potential is termed as cochlear
microphonic. The amount of current (CM magnitude) depends on the forces
exerted upon the hairs, which is ultimately determined by the intensity of the
sound stimulus.
Davis’s variable resistance model is
widely accepted explanation of CM generation. It’s supported by the observation
that changes in CM polarity and magnitude result from experimentally induced
anoxia and electrical currents.
The CM is a graded potential- its
magnitude changes as the stimulus intensity is raised or lowered. This is
showed by the CM input output function. The magnitude of the cochlear
microphonic increases linearly with stimulus level over a range of roughly 60
dB, as is shown by the straight line segment of the I-O function. This classic
figure shows the linear response extending down to about 0.4Mv, but subsequent
studies have recorded cochlear microphonic magnitude as low as a few thousands
of microvolts. With adequate stimulation, the CM doesn’t appear to have a
threshold, per sec; instead the smallest response seems to grow out of the
noise floor, being limited by the recording method, equipment and physiologic
noise.
Saturation occurs as the stimulus
level is raised beyond the linear segment of the I-O function, as shown by the
flattening of the curve. Increasing amounts of harmonic distortion occur in
this region. Raising the intensity of the stimulus even further causes
overloading, in which case the overall magnitude of CM can actually decrease.
The graded nature of the cochlear
microphonic is also observed in terms of the intracellular AC receptor
potential, which is its equivalent measured within the hair cells. In fact,
because these potentials are recorded within a given cell, they enable one to
compare the relative thresholds of the inner versus outer hair cells. Using
this approach, Dallos clearly demonstrated that the inner hair cells are on the
order of 12 dB more sensitive than the outer hair cells.
ü Distribution
of the cochlear microphonic
Recall that large Cochlear
microphonic responses are recorded from round window. This placement was used
extensively by Wever and Lawrence. Similar responses are recorded at the
cochlear promontory. It’s thus important to know what contributes to the round
window response. To study this, Misrahy et al successively destroyed sections
of the guinea pigs cochlea, beginning at the apex and working downwards while
monitoring the cochlear microphonic in the basal turn. They found that the
upper turns didn’t make significant contributions to the cochlear microphonic
in the apical turn. It may thus be concluded that the cochlear microphonic
recorded at the round window is for the most part derived from the activity of
the basal turn.
It’s clear that Cochlear microphonic
magnitude increases with stimulus level for each frequency. Also, the place of
maximum cochlear microphonic magnitude shifts downwards towards the base as
intensity increases. This may at first seem inconsistent with the place
principle. However, the basal shift of the maximum cochlear microphonic
response is probably due to wider range over which the more basal generators
respond linearly. In other words, as stimulus intensity increases, the cochlear
microphonics from the most sensitive place along the basilar membrane becomes
saturated sooner than do the responses from more basal regions. Thus, cochlear
microphonics generated towards the base continues to increase in magnitude when
those from the most sensitive place have already becomes saturated. The place
of maximal cochlear microphonic response therefore shifts downward along the
cochlear partition (upward in frequency).
Thus, the intracellular AC receptor
potential also reveals a changing distribution with respect to frequency when
the stimulus level increases. Here, we see that the tuning of the AC potential
is reasonably restricted around the best frequency when the stimulus level is
low; and becomes wider, extending towards the low frequencies, when the
stimulus level becomes greater. In other words, the intracellular AC receptor potentials resembles a band pass
filter around the best frequency at low levels of stimulation and a low pass
filter at higher levels.
ü Factors
Affecting C.M:
v Anoxia:
It’s caused by occlusion of anterior inferior cerebral artery, damping trachea,
respiration of N2 etc. CM is sensitive to anoxia to some extent. When an animal
dies, the CM magnitude diminishes but doesn’t disappear immediately. It can be
also recorded 4 hrs after death.
v Temperature:
Experiment done by decreasing entire body temperature found that shape of
input-output does not change, only decreases by some amount. Coats (1965) found
no change in CM if the temperature variation is restricted to that region of
the cochlea, using a cold probe.
v Chemical
Environment: Tasaki (1954) framed that injection of isotonic potassium chloride
(increases k+ & decreases Na+) into scala tympani abolished CM, which
demonstrated that CM can’t be maintained if perilymph concentration is changed.
v Intra-cochlear
pressure: Small change causes little change in CM. High ICP has both short term
& long term effect in CM. The changes are reversible and can be permanent
if maintained for a long time.
2)
Summating Potentials (SP):
Summating potentials are composite, made
of a number of bioelectric components. This was first described by Davis,
Fernandez & McAutliffe (1950) & by Bekesy (1950). It appears as a step like
DC shift in potential that lasts as long as the stimulus. It’s the sum of
various components originating in different physiological sites & processes
(Davis et al, 1952, Goldstein, 1954)
The SP can be either +ve or -ve
depending upon the stimulus parameters, recording site, recording techniques
(Dallos et al, 1970). SPs recorded from the scala tympani or the scala vestibule
can be either +ve or –ve & they can reverse polarity, depending on the frequency,
level & duration of stimulus. SPs recorded from the RW tend to be +ve at
low stimulus levels but –ve at high stimulus levels (Margotis et al, 1992).
Honurbia and Ward (1967) measured
the Summating Potential and Cochlear Microphonic simultaneously in each turn of
the guinea pig cochlea, using electrodes located in the scala media. It’s already
that the envelope ( distribution of amplitude along the length of the cochlear
duct) of the cochlear microphonic is a reasonable representation of the travelling
wave envelope. Honurbia and Ward (1975) found that the summating potential was
positive on the basal side of the cochlear microphonic envelope and negative on
the apical side. This result suggests that the summating potential is positive
on the basal side of the travelling wave and becomes negative apical to the travelling
wave peak.
Dallas and colleagues (1941, 1976) used a
somewhat different recording approach, which makes the important distinction
between the average potential of both the scala vestibule and the scala tympani
on one hand and the potential gradient (difference) across the cochlear
partition on the other. This at first complicated distinction is clarified in
the figure. One electrode is in the scala vestibule and the other is in scala
tympani. Each one registers the summating potential at the same cross sectional
plane along the cochlea, but from opposite sides of the scala media.
Subtracting the summating potential in the scala tympani from the summating
potential in the scala vestibule (SV-ST) gives the potential difference of the
summating potential across the cochlear partition. This difference is called
difference component. The average component is obtained by simply averaging the
summating potentials from both scala (SV+ST)/ 2. The average component thus expresses
the common properties (common mode) of the summating potential on both sides of
the scala media.
The DIF component becomes negative
in the vicinity of the peak of the travelling wave envelope, a situation which
resembles the spatial distribution of the positive and negative summating
potential discussed above. The polarity of the average component is essentially
the reverse, being positive around the travelling wave peak and negative
elsewhere.
ü Source
The SP has been thought to arise from
distortion generated by hair cell transaction process. Results obtained from
animals treated with amino glycoside antibiotics suggested that the OHCs may
contribute significantly of the SP at low to moderate intensities, whereas IHCs
may contribute to the SP at higher SPL’s (Dallos 1975). However, recent
experiments with Chinchillas with selective IHC loss (Zheng et al 1997 a)
suggest that IHCs are the major source of SP’s recorded from the round window,
particularly at low to moderate stimulus levels. Animals with a 40-50 % of IHCs
in the base of cochlea showed a 60-80% decrease in SP amplitude at stimulus
levels of less than 80 dBSPL despite having normal CM, normal DPOAE’s & a
normal complement of OHC’s similar results have been obtained from animals with
selective carboplatin induced IHC lesions (Durrant et al 1998) in which lesions
involving both IHC’s & OHCs abolished the SP.
ü Recording
of SP
:
The SP may be recorded in response
to a continuous tone when recorded using a tone burst. This may be seen as a
shift in the baseline of the scala media using a bipolar electrode.
It does not exactly reproduce the
waveform of the stimulus.
ü Characteristics
of SP:
The magnitude & polarity of the
SP are dependent on the frequency and intensity of the acoustic stimulus. At
the best frequency (where the response is largest) the SP is always –ve while
recorded in the scala media as differentially between Scala vestibule &
Scala tympani. This negativity corresponds to excitatory depolarizing activity
of the cochlear hair cells. At frequencies below the best frequency the
polarities of the SP is positive at low to moderate intensities, but reverses
at the high intensities
Davis et al gave streptomycin that
would affect the OHC & found only the –ve SP produced by the IHCs, while
+ve SP & CM are produced by the OHC. At low intensities, SP is more
prominent (because it occurs due to the activity of OHC) but at high
intensities it becomes obscured by –ve SP (which is produced by the IHC’s).
Honrubia & Ward concluded that SP was +ve on the basal end & -ve on its
apical side of the cochlea. It ranges from 0.05 to 0.5 microvolt.
ü Factors
Affecting SP:
v Anoxia
: Konigh et al (1961) identified that SP recorded from scala media immediately
declined & its polarity reversed from –ve to +ve in 40-60 msecs.
During long term anoxia, SP fluctuated
around the 0 point but do not reach a plateau like endocochlear potential &
CM,Upon restoration of oxygen supply to the cochlea, the SP could return to
normally even after prolonged periods of anoxia.
(3) Compound
Action Potentials
The compound action potential
is the extracellular field potential produced by the synchronous depolarization
of a large number of AN fibres in response to a stimulus. It provides the
information regarding functional status of cochlea. CAP reflects not only the
excitation of cochlea but also the excitation of the auditory nerve. It’s
prominent in response transient sounds like clicks and high frequency tone
burst with rapid rise times.
The CAP consists of 2 prominent
–ve peaks, referred to as N1 & N2. The N1 response occurs approximately 1
ms after the onset of the stimulus & N2 appears approximately 1 ms later.
ü Generation
:
The CAP’s can be recorded from an
electrode placed on the RW membrane, placed on cochlear nerve between its exit
from the internal meatus & its entrance to the medulla.
It’s
possible to record simultaneously the CAP and certain of receptor potentials,
the dominant which is the cochlear microphonics. The former placement favours
the CM, whereas the latter favours the action potential. The CM appears first,
followed by the gross action potential. The AP, N1 denote as nerve response
from the first order neurons. It’s of low magnitude due to the fact that the
recording electrode rested on the RW membrane, a locus relatively distant from
the myelinated fibres in the modulus. The N2 depends on the integrity of
auditory nerve. There are 2 different hypotheses postulating that the N2
component of the AP is generated by a second firing of the auditory nerve
fibres while the first firing contributes to N1 peak. The other hypothesis
states that the N2 peak is generated in the cochlear nucleus & passively
conducted to the recording site.
ü Latency
Of A.P:
The latency of the cochlear AP depends
on the intensity & the spectrum of the stimulus sound. The latency of the
AP changes more as a function of the stimulus intensity when the stimulus have
their energy in the low frequency range than the energy of the click stimulus
in the high frequency range.
The decrease in latency as a function of
increasing stimulus intensity has several causes. A nerve fibre discharges when
the excitatory post synaptic potential (EPSP) has exceeded a certain threshold
value. The higher the stimulus intensity the steeper the rise of EPSP & it
does take a shorter time to reach the threshold of firing when the stimulus
intensity is higher. Another cause is related to the fact that the cochlea is
nonlinear. This causes the maximum deflection of the basilar membrane. A shift
of the maximum displacement of the basilar membrane towards the base of the
cochlea results in a decrease of the travel time of the displacement of the BM
to reach maximum deflections. This contributes to the decrease in the latency
with increase in the stimulus intensity.
ü Amplitude
of AP:
The amplitude of AP varies with
stimulus level (Salvi et al, 1979). As stimulus level increases, CAP amplitude
increases over a 40 dB to 50 dB range before saturating & then rolling
over. In addition the latency of the CAP gradually decreases from approximately
2ms at low stimulus levels to approximately 1ms at high stimulus levels.
The lowest SPL at which the CAP can be
detected defines its threshold. CAP threshold for pure tones are generally
15-20 dB higher than behavioural thresholds. This probably occurs because behavioural
thresholds are typically measures using long duration (greater than 200 ms)
stimuli. CAPs are elicited with brief duration stimuli. Longer duration stimuli
are more easily detected than short duration stimuli because of temporal
integration (Gerken et al, 1990). Thus differences in stimulus duration
probably account for the difference between CAP & behavioural thresholds…
ü Clinical
Application:
The amplitude of the peaks can provide an
estimate of the number of auditory nerve fibres contributing to the response
& the width of the CAP can provide an estimate of the synchrony of firing.
A common finding in ears with SN hearing loss is a loss of sensitivity &
decreased amplitude of the CAP. The decrease in amplitude is a reflection of
the reduced number of auditory nerve fibres contributing to the response.
From a clinical perspective, an absence or
greatly diminished CAP in the presence of a robust CM might be indicative of
some type of the neuropathy of the auditory nerve (Starr, 1996). This contrasts
with pure conductive hearing loss, in which CAP input-output function could
simply be shifted towards higher sound levels. i.e although higher stimulus
levels would be required to evoke the CAP, the slope of the amplitude function
could be minimally affected. The latency of the CAP can also be useful in
differentiating between a conductive hearing loss, in which latency is
prolonged & a SN loss, in which latency is normal.
Journal Articles
Centrifugal control
in mammalian hearing - Donald Robertson
The Auditory Laboratory, Discipline of Physiology, School of Biomedical Bio molecular and Chemical Sciences, The University of Western Australia, WA 6009, Australia.
The Auditory Laboratory, Discipline of Physiology, School of Biomedical Bio molecular and Chemical Sciences, The University of Western Australia, WA 6009, Australia.
1. Centrifugal control of
many sensory systems is well established, notably in the γ motor neuron of
skeletal muscle stretch receptors.
2. Efferent (olivo cochlear)
innervation of the mammalian cochlea was first established through anatomical
studies. Histological studies confirmed synaptic terminals in contact with hair
cells and afferent dendrites.
3. Electrophysiology has
elucidated the cellular mechanisms of efferent modulation in the cochlea.
4. The system has potential
roles in noise protection, homeostatic feedback control of cochlear function
and signal processing. There is some evidence in support of each, but also
contraindications.
5. It is concluded that the
role of the olivo cochlear innervation is still contentious, but on balance the
evidence appears to favour a role in enhancing signal detection in noise.
Physiology,
pharmacology and plasticity at the inner hair cell synaptic complex
-
Jérôme Ruel, Jing Wang, Guy Rebillard, Michel
Eybalin, Ruth Lloyd ,
Rémy Pujol and Jean-Luc Puel
Recent neuro pharmacological data at the IHC
afferent/efferent synaptic complex: the type of Glu receptors and transporter
involved and the modulation of this fast synaptic transmission by the lateral
efferents. Neuro pharmacological data were obtained by coupling the recording
of cochlear potentials and single unit of the auditory nerve with
intra-cochlear applications of drugs (multi-barrel pipette). We also describe
the IHC afferent/efferent functioning in pathological conditions. After
acoustic trauma or ischemia, acute disruption of IHC-auditory dendrite synapses
are seen. However, a re-growth of the nerve fibres and a re-afferentation of
the IHC were completely done 5 days after injury. During this synaptic repair,
multiple presynaptic bodies were commonly found, either linked to the membrane
or “floating” in ectopic positions. In the meantime, the lateral efferents
directly contact the IHCs.
References
1. BERLIN, Charles.I Neurotransmission
and hearing loss: Basic Science, Diagnosis&Management (1997).
2. MILAN, F.Grandori Advances in Audiology, Vol-7-Cochlear
Mechanics (1990)
3. SCHOUTEN, M.E.H Auditory processing of speech from sounds
to words (1992).
4. BACON, Sid.P Compression: From cochlea to Cochlear
Implants (2004).
5. BERLIN, Charles I, HOOD, Linda.J Hair Cell Micromechanics
and otoacoustic emissions (2002).
6. THOMAS R Van Clinical aspects of hearing (1996).
