Lecture 15 Hearing II Flashcards
Central auditory nerve processing activity allows for the perception of…….
These functions (culminate in perception of subtle speech nuances) allow for…
Loudness (intensity), pitch(frequency) and sound direction.
Social communication and sound localisation
The central auditory pathway
Auditory pathways compared to visual pathways and why
Spiral ganglia -> auditory complex (temporal lobe) -> hearing, speech, language centres overlap.
More complex than visual -> more relay nuclei from peripheral organ (cochlea) to cortex, several alternative pathway from cochlea to auditory cortex
Describe the complicated central auditory pathway
{Draw mindmap for this with card 4}
Spiral ganglion (1° auditory neurons) -> auditory nerve -> ventral cochlear nucleus [dorsal cochlear nucleus] -> superior olivary complex (1st relay station) -> ipsilateral superior olivary complex [contralateral superior olivary complex] -> lateral lemniscus -> inferior colliculus (midbrain) -> medial geniculate nucleus (thalamus) -> auditory complex (final & complex sound analysis - determine sound complexities)
-> contact superior colliculus : integration of visual & auditory info
Three features of central auditory pathways and examples
1. Other projections and brain stem nuclei contribute to auditory pathways.
2. Extensive feedback in auditory pathway
3. Auditory nuclei in brain stem receive input from both ears
- DCN - straight to inferior colliculus. Inferior colliculus receives input from DCN and VCN
- Superior olivary complex: neurons send efferent innervation to stimulate OHC
Auditory cortex: send info to MGN & inferior colliculus - Starts from superior olivary complex
Analysing sound frequency in auditory nerve
- increased intensity means
- characteristic frequency is
- increased firing rate
- highest response to a certain frequency. (That frequency has most number of spikes due to higher firing rate)
Stimulus intensity depends on
The firing rate of a given neuron and the number of neurons firing.
(More movement of basilar membrane, more sensory hair cells activated, more neurons employed, higher intensity)
- higher frequency - higher basilar membrane movement
- lower frequency - lower basilar membrane movement
Frequency encoding at
- very low frequency
- intermediate frequency
- high frequency
- phase locking (response of each neuron at every cycle. AP fired at a consistent part of the wave.)
- volley principle (phase locking + tonotopy ) [response phase locked not at every cycle but is constant - ex. Every 4 cycles]
- rely exclusively on tonotopy (AP fired randomly, irregularly. Cannot analyse sound frequency).
Sound localisation is important…..
How many ears are needed for sound localisation on the horizontal plane compared to the vertical plane?
…to know where the sound is coming from
Horizontal: both ears , Vertical: one ear enough
What are the two processes used for localising sound on the horizontal plane?
Explain the processes
Interaural time delay (low frequency - 20-2000Hz).
- analysed by specialised neurons in SON.
- experienced when sound comes at you at angle between 45° and 90°.
- sound from right: reach right ear, after delay left ear.
- sound in front no delay
Interaural intensity difference (high frequency - 2-20kHz)
- sound shadow cast on area opposite from where sound comes from. (The ear (sound shadow) -> softer sound)
- high frequency sound so no tell difference of sound waves
How is Interaural time delay analysed in the SON
Binaural neurons in SON (1st relay station) receive info from both ears -> analyse time delay with low frequency sound.
delay time and interaural time delay
If sound is coming from the left ear, how is this sound analysed by the SON for interaural time delay?
Activity initiated in left cochlear nucleus -> synaptic activity sent to SON by auditory nerve.
Sound reach right ear -> synaptic activity stimulated in right cochlear nucleus. First impulse (left ear) travelled further.
Both impulse will the reach the same neuron in SON -> sum of synaptic potential generates AP -> signal that sound from left.
What are the neurons that are responsive to high frequency sounds in the superior olivary nucleus?
What are their characteristics?
- Type excitatory- excitatory neuron (EE): respond (highest firing rate) with excitation from contralateral and ipsilateral ear.
- Type excitatory- inhibitory neuron (EI): excited by sound from contralateral ear & inhibited by sound from ipsilateral ear.
-sensitive to intensity, present in auditory cortex and pathways, anatomical basis of sound localisation processes on horizontal plane
How is sound localized on the vertical plane?
The sound difference between direct and reflected sound is analysed. Each difference is analyzed on vertical plane and know if sound above or below
External ear : bump & ridges - reflect sound
The primary / secondary auditory cortex
Function and features
- most complex sound analysis occurs with highest level of frequency and intensity tuning (neurons in really nuclei [auditory pathway] analyse sound info [intensity, frequency, localisation]. Higher the relay nucleus, more complex analysis)
- high frequency sounds located medial, low frequency sounds located lateral
What is the ice cube model
Shows how complex sounds are analyzed by 1°A cortex.
What is audiometry?
What are the two categories of methods ? Define them
It is used to measure hearing thresholds and auditory responses of a person
Objective methods
- based on various stages of electrical activity recordings from cochlea to cortex.
- auditory potentials reflect many neural pathway electrical activity that code sounds
Subjective methods
- cooperation of individual needed
- based on subject response and perception of sound
- Pure tone audiograms used - determine auditory threshold at each frequency
- Two ways of objective audiometry methods
- What is electrocochleography
- Define Brainstem Auditory Evoked Potentials (BAEP)
- Individual unitary potentials - directly recorded from single nerve fibre/ cell
Compound potentials - record at distance from origin, reflect unit potentials sun - Recording of compound cochlear nerve action potential at round window. Recording electrode placed near tympanic membrane.
- Recoding electrode placed at skull. One ear stimulated with sound, electrical potential recoded from brainstem. Humans rely on wave with highes amplitude.
What are the causes of hearing loss
Drug- induced hearing loss (ototoxicity drugs)
Noise- induced hearing loss (acute/chronic sound exposure)
- middle or inner ear damage, genetic or non genetic
Age-related hearing loss (most common)
Loss of outer hair cells
1. What happens when OHC are lost
2. How are they damaged
3. The result of this OHC loss
4. How can it be aided
- Incomplete deafness
- More vulnerable to oxidative stress
- Loss of cochlear amplification so 40 -50 dB hearing loss & loss of high cochlear sensitivity and frequency discrimination
- Hearing aids but cannot restore speech discrimination fully
Loss of outer hair cells and IHC
1. What happens when OHC and IHC are lost
2. The result of this pathology
3. How can it be aided
- Complete deafness
- Organ of Corti collapsed and scars replace sensory cells
- Cochlear implants because nerve fibres are still working and can directly stimulate them. Hearing aids would not help.
What induces amnoglycoside ototoxicity?
What does it lead to?
Streptomycin and gentamicin
Loss of sensory hair cells staring with first OHC layer which can lead to mild hearing loss, then incomplete deafness and complete deafness
Describe how noise trauma causes hearing loss
- environmental factor , acute/chronic noise exposure
- cause permanent (complete deafness) or temporary (restorable) hearing loss
- lead to glutamate excitotoxicity
What is OHC and IHC sensitive to respectively?
What is OHC sensitive to?
What happens to IHC when here is high level of noise
Both: noise
OHC: oxidative stress -> apoptosis
IHC: excessive glutamate release -> glutamate excitotoxicity -> damaged synaptic region
Glutamate excitotoxicity
- What does it do?
- How does it do it?
- How can it be reduced?
- Disrupt synaptic ending -> disable auditory neurotransmission
- Noise exposure -> IHC release excessive glutamate (prolonged/ multiple exposure)-> NMDARs activated by glutamate -> Ca2+ entry into postsynaptic endings -> apoptotic pathways activated & swelling -> injury and death
- Antioxidant, NMDAR antagonist application before noise exposure
How does oxidative stress induce hearing loss
Free radicals break down lipid and protein molecules, damage DNA and trigger cell death in cochlea
Describe presbyacusis
- deafness by ageing
- start at high frequency to low frequency
- eventually conversation area affected
- impaired sound localisation and auditory processing
