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CMSD5280 Audition ll > Cochlear Physiology IV: Auditory Nerve > Flashcards

Cochlear Physiology IV: Auditory Nerve Flashcards

HC innervation and Categorization (69 cards)

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1
Q

Review of the main parts of the cochlea:

A
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2
Q

Where are the low and high frequencies located in the auditory nerve fiber?

A

To form the auditory nerve bundle, low-f ANFs are inside (medially), high-f ones are peripherally located (Laterally)

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3
Q

What does this image show?

A

Frequency distribution of the frequencies in the ANF shown as CF changes with location

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4
Q

What are the two types of afferent neurons and to which HC are they associated?

A

Type1 : IHC
Type 2: OHC

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5
Q

What are the important characteristics of IHC?

A

Correspond to the inner radial fibers connected to IHC

50,000 afferent neurons in the cat, and about 30,000 in man

95% type I. Compare to the number of IHCs

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6
Q

What are the important characteristics of type 2 ANF of OHC? (3)

A

Pseudomonopolar,
Unmyelinated
Less knowledge

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7
Q

Where do the auditory afferent and efferent nerves in OC pass through?

A

Both afferent and efferent pass through Habenula perforate

Efferent OHC goes across the TC

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8
Q

What is the ratio of Type l and Type ll SGN on IHC and OHC?

A

Type I SGNs to IHCs: radial fibers, convergent innervation:>10 SGNs to one IHC, each SGN one synapse with one IHC,

Type II SGNs to OHCs: outer spiral fibers, divergent: one SGN to > 10 OHCs, each SGN synapse with many OHCs

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9
Q

What do we know about the synapse and myelin sheet of HC in the OC?

A

SGN fibers under HCs have no myelin sheath. Unmyelated in OC

Synapses with HCs at their bottom surface.

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10
Q

What do we see from this image related to ribbon synapses? (2)

A

Ribbon synapses between SGNs and both IHCs and OHCs.
Afferent Type : Bottom of IHC Presynaptic ribbon bigger and oriented toward modiolar side

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11
Q

Ribbon synapses are found in _____________ and the ______________

A

cochlea and retina

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12
Q

What is the anatomical feature of ribbon synapses?

A

ribbon or presynaptic dense body

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13
Q

What are the two functions of ribbon synapses?

A

High speed: of neurotransmitter release—temporal coding (less important)

long-lasting release for continuous sound - (more important)

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14
Q

What makes ribbon synapses different than conventional synapses?

A

Difference from conventional synapses: anatomy and function

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15
Q

What are the three sequences of the vesicles from the retina ribbon image?

A
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16
Q

What are the differences in shapes of the ribbons in the retina and those in IHC?

A

Ribbons in retina cells shape like horseshoe, those in IHCs shape like American football

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17
Q

What is ribeye and why is the reason it is called this way?

A

The ribeye forms the protein structure of the ribbon named after the shape of the ribeye piece of steak.

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18
Q

What is the role of AMPAR?

A

α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid(AMPA) receptor:
It is an ionotropic transmembrane receptor for glutamate that mediates fast synaptic transmission for action potentials.

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19
Q

What is NMDAR?

A

NMDAR: N-methyl-D-aspartate (NMDA)receptor, not related to AP generation, but slow, long-term effects.

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20
Q

What forms the backbone of the ribbon?

A

A- domain

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21
Q

What is Piccolino?

A

Protein in the ribbon, smaller version of Piccolo, don’t know the function.

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22
Q

What is Otoferline?

A

Located downside of ribbon with connection to presynaptic zone

Otoferline and adaptor protein work together to fulfill special function

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23
Q

What is Bassoon?

A

the anchoring protein of ribbon to keep it close to the active zone same protein as the common conventional synapse

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24
Q

What is the vesicle?

A

Around the zone, can be classified,
Closer to the zone faster release to help in faster release of NT, they are more ready

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25
What are CaV1.3?
CaV1.3 Special calcium channels in presynaptic region
26
What is the difference between Ribeye A-Domain and Ribeye B-Domain?
Ribeye A; ribbon frame Ribeye B: active components for holding vesicles
27
What are the special proteins for cochlear ribbon synapses? (3)
- CaV1.3, specific L-type Ca2+ channel - Otoferlin - Piccolino - several proteins common for conventional synapses are missing from ribbon synapses
28
What are special features in HC ribbon synapse related to Synaptotagmins 1/2, synapsins, synaptogyring complexins and SNAREs (including SANP-25) , Munc 13, CAPS?
The proteins are missing Those proteins are important for neurotransmitter release in conventional synapse
29
Since ribbon synapses aren't conventional synapses, what is the importance of proteins like Otoferlin and adaptor proteins?
They are specifically seen in IHC-SGN ribbon synapses and add special features that are not seen in conventional synapse
30
What makes the proteins in ribbon synapses special mechanisms for NT?
There are special mechanisms for NT including: 1. The process of vesicle trafficking/replenishment 2. Tethering, docking and fusion 3. Probably recycling (via endocytosis).
31
What makes the proteins in ribbon synapses special mechanisms for NT?
There are special mechanisms for NT including: 1. The process of vesicle trafficking/replenishment 2. Tethering, docking, and fusion 3. Probably recycling (via endocytosis).
32
What are two proteins to remember from special features of HC ribbon synapse?
Piccolino and Otoferlin
33
What is the difference between Piccolo and Piccolino proteins?
Piccolo (>500 kDa) is truncated as piccolino (350 kDa) in ribbon synapses, unknown function
34
What is the main functional feature of ribbon synapses compared with conventional synapses?
* Fast and long-lasting release of NT, requiring fast recycling (conventional synapse don’t have such functional features) If we lose these features, there will be loss of hearing
35
What are NT release in ribbon synapses facilitated by? (4)
Large “Ready to release pool (RRP)” of vesicles hold by ribbons The number and distribution of CaV1.3 channels Special Mechanisms for exocytosis across ribbon synapse (related to otoferlin) Special mechanisms for vesicles replenishment and endocytosis (neurotransmitter recycle)
36
What is the main NT for IHC-SGN?
Glutamate
37
How do we know that glutamate is the main NT in IHC-SGN?
To judge if a molecule is a NT there are 4 criteria in total Glutamate—meet most of the criteria: 1. Glutamate is an amino acid existing every cell, rich in vesicle (criterion i) 2. Glu can be released from synapse, agonism can activate action potentials in AN (ii). 3. Action potential can be blocked by special blocker against AMPAR (criterion iii) 4. It is not fully understood how the released glu can be removed (criterion iv): (1) by glial cell, and (2) by endocytosis
38
What did the bassoon research on Mutant mice was about? (2)
Evidence for Ribbons on fast response This research did not target the ribbon proteins but instead target Bassoon because they are difficult to target. The animal can survive when we lock out on Bassoon
39
What were the results of the Bassoon research on mutant mice? (3)
* In this mutation, <3% IHC-SGN synapses retained anchored ribbons * AN has normal threshold, dynamic range, post-onset adaptation to tone bursts, phase lock * Rate decrease (driven and spontaneous), increased variance of first-spike latencies
40
What is shown in this picture?
Results of Lockout of Basson. IHC we have more than 10 presynaptic ribbon after mutation we lose most
41
What is shown in this graph?
Delayed and reduced onset response in mutated mice—suggesting the role of ribbon in quick response
42
What are the differences between A B and C?
Evidence of Ribbon being important for lasting response and coding of sounds A: decreased peak rate and peak/adapted rate ratio. B: delayed peak latency and peak rate to clicks. B: Longer peak latency in mutated samples in response to click (transient signals) Evidence to increase latency to quick change in signal C: Lost response variation across signal with different transient feature. The order of signal transient is: click > pip>tone with reduction of transient, peaks decrease in normal animals but in mutated animals there is no more difference so no preference in the transients of signals After the experiment, the animal can still hear sounds but delayed and reduced response to the onset of signal with the loss of Bassoon.
43
What do neurons code in a signal? (3)
Frequency Intensity Temporal pattern
44
What are the three ways neurons code signals?
Rate change Place code Temporal coding (phase locking)
45
What do these graphs represent? (2)
Tuning curve representations of the Frequency selectivity of Hair Cells The tunning curve is point test and it is measured across the entire envelop
46
What is the response area?
An area defined by intensity and frequency, imaginary area. Any area above tunning curve is called the response area.
47
Why is the tuning curve sharper at high frequency side? (2)
When the BM vibration peak move slightly towards basal turn (when stimulus fre. Increase), the vibration at CF location drop quickly, because the envelope is sharp at low frequency side.
48
What does this graph show?
Shifting of sti Fre away from CF, vibration at CF will be lower than threshold. To reach the threshold at CF, sound level must be increased. For the same amount from Fre shifting, low fre shift requires less increase in sound level because the envelop is shallower high frequency side Asymmetrical pattern of BM, Shallow slop at high frequency side Big left blue triangle: Need to increase high frequency signal by that much to be perceived at the CF toward apex Mid green triangle: Need to increase low frequency signal by that much to be perceived by the CF toward high frequency side
49
Explain Frequency Selectivity of Auditory nerves:
Each auditory nerve works as a bandpass filter Better selectivity at low intensity Quantitatively measured as Q value: e.g. Q10 dB = CF/bandwidth (BW) of TC The higher the Q value, the better the frequency selectivity Tuning Curve spreads to low-frequency side as a tail at high intensity CF tip needs active mechanism of OHCs
50
How do you quantify Frequency Selectivity?
Q values Tuning curves with the same CF can have different BW BW: Bandwidth Q10dB = CF/BW10 dB The larger the BW, the lower the Q value Lower the BW, better the frequency Selectivity
51
What does this graph show?
The distribution of the characteristic frequency along the cochlea
52
In the comparison of the tuning curves, why is frequency in logarithm?
The graph shows Tuning Curves of different Neurons Octaves ratio scale: Compare the distance along the BM is not the same because 1 octave will cause high distance along BM as you measure So, if bandwidth of TCs is measured in octave, it will decreased with CF.
53
What does this graph show?
Bandwidth change along cochlea where the high frequency is shown to be better
54
Why is the cochlea mapped by frequency in logarithm? (3)
Bandwidth increases with CF in linear scale. This does not indicate poor frequency selectivity at higher frequencies! JDD for frequency (in octave) covers a shorter distance at high frequency region. Frequency selectivity better measured with Q10, which is bigger at high frequency.
55
Why do we use Q to describe frequency along the BM? (4)
1. BW is inversely related to frequency selectivity. Larger the BM, poor Frequency selectivity 2. CF should also be considered. 3. Q value is a ratio, putting CF into the consideration of frequency selectivity (similar to Weber’s fraction). 4. Larger the Q, better the frequency selectivity
56
What is a Spontaneous rate of an ANF? (3)
Most fibers have (rate) thresholds within 20-40 dB above the absolute threshold Smaller amount spread to 60-80 dB above abs threshold only for less than 10% of fibers (Low spontaneous rate) Nerve fibers with high thresholds often have low spontaneous spike rate and often receive stronger efferent inhibition on their terminals with IHCs (Inhibition we don’t know the function)
57
What is the difference between the LOW and HIGH SR (Spontaneous Rates)?
In ANFs, lower group Neuro fibers have close to 0 spontaneous rate which means fire less easily if not High intensity sound
58
What is the difference between groups of ANF synapse IHC at Modiolar side vs. Pillar side?
On modiolar side: large ribbon, small terminal, low SR, high threshold larger dynamic range (encoding in noise) More sensitive to noise damage (Exposed to higher sound will cause damage) Those groups of neurons are more related to background noise Smaller Terminals Bigger Ribbons On Pillar side: small ribbon, large terminal, high SR, low threshold
59
What are the 3 functional differences of the mechanisms for spatial difference?
Shape, size of ribbons, Ca channels related to vesicle release Recycle for threshold
60
What are the mechanisms for the spatial difference for noise damage? (3)
Glutamate-aspartate transporters (cleaning) reason for noise induce synaptical damage Most likely to occur at Modiolar sides Number of Ca ch per synapse and ribbon size for vesicle release GluR at postsynaptic membrane
61
What does this graph demonstrate?
Rate-level function of high-SR ANFs and the concept of dynamic range Results of higher SR ANF at the CF of the neuron. Initially above the threshold will cause higher increase of rate then will gradually get saturated Between the threshold and Saturation = dynamic range Dynamic means change in input = change in output Dynamic range in this graph: around 20 dB to 40
62
What are Saturated RLF?
Seen from ANFs with high SR (HSR) It is called typical, because HSR ANFs are the majority (~90%) Those ANFs have low threshold, narrow dynamic range, most likely responsible for auditory sensitivity. They may not be able to code high level sound
63
What does this graph demonstrate?
The impact of signal frequency vs CF on RLF of high-SR units This kind of TLF is typically seen at the CF. The CF of this neuron is 2.1 At higher and lower Sr Only seen around CF because related to OHC mechanism, can only be active at CF tone at lower frequency If not will get saturated at higher intensity because of the Amplification mechanism
64
What do these graphs demonstrate?
RLF comparison across SR groups: a, b and c for H, M and L SRs—all at CFs Higher SR, more significant saturation Lower SR units, you see no saturation
65
What are the three methods to examine temporal pattern?
Post (or peri) stimulus Time Histogram (PSTH) PRH—period histogram Interspike interval histogram
66
How does the PSTH work?
After the onset of the stimulus, count the number of spikes in each time bin Time bin- have equal time durations (i.e. 1-5 ms) to demonstrate the time change The number of spikes in each bin represents the prevalence of neural firing with respect to the stimulus
67
What does the PSTH show in this situation?
Each black bar is a time bin. The PSTH shows a response that goes through five stages: Onset peak, fast then slow adaptation, offset depression, and recovery How to observe the time change of Neuron response: Fast onset peak: Neurons response to the onset of sounds Before Onset: You have more After onset: Decline because they need to rest, less synchronized (Fast-Slow adaptation) Offset If you turn off the sound, the response of neurons will quickly drop
68
What is phase locking?
The temporal processing of ANFs ANFs fire at a specific phase of the sound. When the sound frequency is low, one ANF can fire to every sound cycle. With increasing frequency, firing will skip: and not occur in every cycle. More likely to be seen at certain phases At increasing frequency, neurons may show fewer spikes (Phase locking)
69
What does this graph show?
The Recording from one ANF usually need sweeps of many times to show phase locking Random spikes due to SR at a lower rate Increase frequency, increases the response of neurons but you will expect it less at the same phase because of phase locking,

CMSD5280 Audition ll (19 decks)

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