BIOLOGY 2D03 Lecture Notes - Cranial Nerves, Gene Duplication, Superior Temporal Sulcus

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28 Jan 2013
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Lecture 1: Hair Cells
Sound is pressure waves of alternating compressions and rarefactions. It’s characterized by
intensity, frequency, and direction.
Intensity is in decibels Sound Pressure Level: dB SPL = 20 log [P/P0]. This is relative to an
absolute reference. Huge range of sounds are encountered in the world. Human hearing
spans 20 – 10,000 Hz, with peak sensitivity at 2 kHz.
90dB can produce temporary threshold shift, in which sensitivity is reduced. With severe
sound exposure, cochlear hair cells can be killed. They don’t regenerate. Other hearing loss
may be iatrogenic (gentamicin). Most common hearing loss is presbycusis, or loss of high
frequency hearing with age.
The pinna collects sound, amplifying it. The ear canal resonates frequencies around 4 kHz
and enhances them. These structures help you locate the source of a sound based on
frequency signatures.
The middle ear bones muse overcome the acoustic impedance mismatch of air/water. Water
has much higher acoustic impedance, and normally sound going from air to water is mostly
reflected. The small area of the stapes footplate and lengths of middle ear bones (lever)
increase the pressure wave ~26 fold.
Tensor tympani and stapedius attenuate transmission through the middle ear when noise is
really loud.
A loss of middle ear function is “conductive” hearing loss. It may be caused by otosclerosis,
in which bony growth impedes the ear ossicles. Sensorineural hearing loss may be due to
loss of hair cells. They can be differentiated by using bone conduction through the skull to
test for an inner ear response.
External hearing aids may help with both conductive and sensorineural hearing loss. For
some conductive hearing loss surgery helps. For severe sensorineural hearing loss, a
cochlear implant may be necessary.
Movement of stapes footplate at oval window vibrates the scala vestibuli. Scala vestibuli on
top, bordered below by Reissner’s membrane, below which is scala media (bounded below
by the apical surface of the hair cells). There are inner (1 row) and outer hair cells (3 rows).
At the bottom of the scala media is the cochlear partition (hair cells, basilar membrane and
tectorial membrane). Below this is the scala tympani.
Scala vestibule and tympani have perilymph (low K, high Na), scala media endolymph (high
K, low Na). Endolymph is secreted into the scala media by the stria vascularis on its outer
wall. Hair cells’ apical surfaces are bathed in endolymph, their basolateral surfaces in
perilymph. The apical surfaces have tight junctions to maintain concentration barriers and
the +80 mV endolymphatic potential compared to the perilymph. These two forces drive K
ions into hair cells at their apical surfaces.
Meniere’s disease occurs with disrupted endolymphatic fluid circulation and results in
sensorineural hearing loss. Vestibular dysfunctions also occurs.
Vertical movement of the basilar and tectorial membranes causes shear between them,
pushing stereocilia (actin filled microvilli) on hair cells from side to side. Hair cells have 1
true cilium called the kinocilium, but it is absent in the adult cochlea. A tip link runs from
the top of 1 stereocilium to the side of the adjacent taller one.
Deflection toward the taller stereocilia results in stretching of the tip link and opening of ion
channels at the tips of stereocilia. Deflection in the opposite direction closes channels (at rest
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10% are open). The channels are cation-permeant, though the [K] differential and
endolymphatic potential lead to a flux of mostly potassium into the hair cell from its apex.
This depolarizes the cell. Sinusoidal deflections of the cochlea result in sinusoidal changes
in hair cell membrane potential.
During a sustained deflection of hair cells, the ion current decays in a form of adaptation. A
hypothesis is that motors move the attachment of the tip link to relieve the mechanical
activation.
Hair cell depolarization leads to opening of VG Ca channels that trigger fusion of vesicles
containing glutamate. These excite AMPARs on afferent fibers which carry signals to their
cell bodies in the spiral ganglion. VG K channels in the basolateral surface of hair cells
allow an outward flux of K, and return the cell to its resting potential (hyperpolarizing it
really).
At rest, hair cells release glutamate and afferent neurons have spontaneous activity. So, you
can signal by increasing or decreasing the firing rate. An individual cochlear afferent only
synapses with a single inner hair cell. At the synapse, the hair cell has a synaptic ribbon to
facilitate vesicle release.
There are 3 outer hair cells for every inner hair cell, but 95% of afferent fibers go to inner
hair cells via type I fibers. The contralateral superior olivary complex gives off a crossed
olivo-cochlear bundle that synapses massively on outer hair cells. This pathway is
inhibitory, and when it inhibits the outer hair cells it causes a loss of sensitivity and
frequency selection in afferent signals from the cochlea. So inhibiting the OHCs alters the
response of the IHCs.
When depolarized, OHCs shorten and when hyperpolarized they lengthen. This
electromotility is thought to be carried out by the anion channel prestin, which may be
translocated with changes in membrane potential and altering the membrane area. This
contributes to the vibration of the cochlear partition and enhances the motion detected by
inner hair cells.
One form of evidence for this idea of active biological motors is that the ear can generate
sounds called otoacoustic emissions, which are echoes or distortion products occurring with
certain stimulation. Distortion product otoacoustic emissions (DPOAEs) reflect normal
activity in the OHCs of the cochlea and may be used to diagnose sensorineural hearing loss.
Efferent innervations of the cochlea suppresses cochlear sensitivity by inhibiting OHCs. The
olivo-cochlear efferents release ACh on the OHCs. The OHCs have a unique nicotinic
AChR. This receptor allow a Ca influx and depolarizes the OHC. But nearby Ca-gated K
channels immediately open and hyperpolarize the cell.
Hopefully this unique AChR will provide specific drug targets for the auditory system.
Lecture 2: Auditory I
If you try and mask one tone with another, the farther apart the frequencies are the louder the
masking tone has to be to have an effect (the effect being that you can’t hear the other tone).
The identity of a sound is largely conveyed by its frequency content. The frequencies present
in the different vowel sounds, for example, show amplification and attenuation of the sound
produced at the vocal folds at varying frequencies. These are seen in spectrum plots, which
show energy content vs. frequency.
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The high energy peaks in a spectrum plot are called formants. Vowels are defined by their
first two formants (the first two resonant peaks in their spectra). So, frequency plays a role in
determining pitch as well as quality of a sound.
The cochlea and the downstream auditory transduction are tonotopic, breaking down sounds
into their component frequencies. Outer hair cells in the cochlea function to amplify sound
and sharpen tuning to help you discriminate between frequencies. The OHCs show level
dependent amplification and amplify softer sounds more. You can also discriminate between
frequencies better at lower sound levels, since loud sounds elicit responses over broader
ranges of frequencies.
With OHCs destroyed, you require a much louder sound to move the basilar membrane.
There is little difference with very loud sounds though, because loud sounds aren’t amplified
much by OHCs. This feature of amplification of softer sounds provides “compression,” so
that the same range of response in the cochlea occurs in response to a larger range of sound
levels.
Each auditory nerve fiber is tuned to be most sensitive to a narrow range of frequencies. Its
“best frequency” is the one to which it is most sensitive. Different fibers are tuned to
different frequencies.
A tuning curve is a representation (threshold sound level vs. frequency) of how much sound
is needed to induce a response in an auditory nerve fiber at different frequencies.
Hearing loss may be categorized as: Conductive (loss of middle ear transmission), Metabolic
(damage to stria vascularis or cells supporting hair cells), Sensorineural (damage to hair
cells), of Central (tumor or lesion in auditory nerve or CNS).
Inner hair cells transduce the vibrations into nervous signals in the auditory nerve. Damage
to IHCs reduces the sensitivity of auditory nerve fibers.
Outer hair cells increase sensitivity and sharpen frequency tuning of auditory nerve fibers.
Damage to OHCs results in reduced sensitivity (requiring louder noise to reach threshold)
and stimulation by a broader range of frequencies.
These types of sensorineural hearing impairment produce the following problems:
oSoft sounds can’t be heard, due to a shift in the sensitivity (threshold).
oSounds become louder faster (loudness recruitment), and in some cases any audible
sound may be too loud. This is because the volume at which sound becomes
uncomfortable remains the same, but the threshold to hear softer sounds may be greatly
increased.
oYou can’t separate sounds by frequency as well since there is a decreased frequency
resolution (widened tuning curves). This causes the sound to be muffled.
Hearing loss often occurs more at higher frequencies, with auditory nerve fibers located near
the base of the cochlea.
Genetic deafness may be syndromic with other associated non-cochlear symptoms, or they
may be non-syndromic in which case they only have cochlear phenotypes. One gene for
non-syndromic deafness is the gene for prestin, the OHC motility motor.
Another non-syndromic gene is DFNB1, which encodes for connexin 26 and 31, proteins
which form gap junctions. They are thought to play a role in potassium recycling from the
perilymph back into the endolymph (by going from the scala tympani to the stria vascularis).
The connexins aren’t present in hair cells themselves. They play a role is maintaining the
[K] gradient and the endolymphatic potential of +80 mV.
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