BIOC32H3 Lecture Notes - Lecture 16: Perilymph, Vestibular Nuclei, Intention Tremor
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Inner ear —cochlear-basilar membrane has a non uniform stiness to it. Regions
close to oval window is sti. Stiness comes from the fact that there are a lot of
collagen bres in that region. In order to get that area to vibrate due to stiness
need high frequency vibration. Low frequency vibrations will only cause aect at
opposite end. Key to hearing in basilar membrane. When we think about sounds
we can't hear then, it comes from the fact that stiness of the membrane, you
would need an even greater amount of stiness of membrane for very high
frequency (availability of stiness 'key').
Bending of hairs causes K channels to open, instead of leaving, it enters cell and
triggers depolarization so that Ca2+ can enter in hair cell. They are releasing
glutamate , and so depolarization occurring in auditory neuron and so frequency
of sound occur.
Hair cells are dierent lengths (range) therefore if soft sound, only push tallest
hair in tectorial membrane, and only few channels opening up, and so moderate
everything. Loud then lots of hair pushed even small ones, and lots of everything,
action potential frequency therefore higher.
Dierent frequencies of action potential correspond to the loudness of the sound.
Superior olivary nucleus which is involved in sound localization, collect info from
both left and right ear and localize where that sound is coming from. Uses delay
to localize where sound is coming from.
Superior olivary nucleus both contra lateral and ispsilateral.
Conductive hearing loss is failure of sound to be conducted from external
environment to inner ear, due to block way or Lessing to pathway (ear mus,
buildup of wax, 1uid buildup due to ear infection for example).
Sensory neural hearing loss is whose origin could be traced to the inner ear
mostly, rarely to auditory brain cortex/nerve problem.
High frequency are most susceptible to loss is due to chronic exposure.
Mechanical damage to hair cells, constant pushing/bending of hair could break.
Once lost they are lost. No longer gated channel, and not much depolarization
and won't hear sound well.
Very loud sound then hair cells bend violently and so break o.
If we have glutamate released and AMPA and NMDA being triggered by binding of
glutamate, and so in1ux of CA2+ but chronic elevated levels of it then cell begins
to degrade (excitotoxicity).
Study done on guinea pigs, that made them to listen to ear damaging sounds,
and found that hearing damage could be lessened by injecting glutamate
antagonist (kynurenate). Therefore exposure to loud sounds we are inducing
excitotoxicity by constant release of glutamate. By blocking it we can lessen it.