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

Cochlear Physiology IV: Auditory Nerve Flashcards

HC innervation and Categorization

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
Q

What are CaV1.3?

A

CaV1.3 Special calcium channels in presynaptic region

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26
Q

What is the difference between Ribeye A-Domain and Ribeye B-Domain?

A

Ribeye A; ribbon frame
Ribeye B: active components for holding vesicles

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27
Q

What are the special proteins for cochlear ribbon synapses? (3)

A
  • CaV1.3, specific L-type Ca2+ channel
  • Otoferlin
  • Piccolino
  • several proteins common for conventional synapses are missing from ribbon synapses
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28
Q

What are special features in HC ribbon synapse related to Synaptotagmins 1/2, synapsins, synaptogyring complexins and SNAREs (including SANP-25) , Munc 13, CAPS?

A

The proteins are missing
Those proteins are important for neurotransmitter release in conventional synapse

29
Q

Since ribbon synapses aren’t conventional synapses, what is the importance of proteins like Otoferlin and adaptor proteins?

A

They are specifically seen in IHC-SGN ribbon synapses and add special features that are not seen in conventional synapse

30
Q

What makes the proteins in ribbon synapses special mechanisms for NT?

A

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
Q

What makes the proteins in ribbon synapses special mechanisms for NT?

A

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
Q

What are two proteins to remember from special features of HC ribbon synapse?

A

Piccolino and Otoferlin

33
Q

What is the difference between Piccolo and Piccolino proteins?

A

Piccolo (>500 kDa) is truncated as piccolino (350 kDa) in ribbon synapses, unknown function

34
Q

What is the main functional feature of ribbon synapses compared with conventional synapses?

A
  • 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
Q

What are NT release in ribbon synapses facilitated by? (4)

A

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
Q

What is the main NT for IHC-SGN?

A

Glutamate

37
Q

How do we know that glutamate is the main NT in IHC-SGN?

A

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
Q

What did the bassoon research on Mutant mice was about? (2)

A

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
Q

What were the results of the Bassoon research on mutant mice? (3)

A
  • 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
Q

What is shown in this picture?

A

Results of Lockout of Basson. IHC we have more than 10 presynaptic ribbon after mutation we lose most

41
Q

What is shown in this graph?

A

Delayed and reduced onset response in mutated mice—suggesting the role of ribbon in quick response

42
Q

What are the differences between A B and C?

A

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
Q

What do neurons code in a signal? (3)

A

Frequency
Intensity
Temporal pattern

44
Q

What are the three ways neurons code signals?

A

Rate change
Place code
Temporal coding (phase locking)

45
Q

What do these graphs represent? (2)

A

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
Q

What is the response area?

A

An area defined by intensity and frequency, imaginary area. Any area above tunning curve is called the response area.

47
Q

Why is the tuning curve sharper at high frequency side? (2)

A

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
Q

What does this graph show?

A

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
Q

Explain Frequency Selectivity of Auditory nerves:

A

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
Q

How do you quantify Frequency Selectivity?

A

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
Q

What does this graph show?

A

The distribution of the characteristic frequency along the cochlea

52
Q

In the comparison of the tuning curves, why is frequency in logarithm?

A

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
Q

What does this graph show?

A

Bandwidth change along cochlea where the high frequency is shown to be better

54
Q

Why is the cochlea mapped by frequency in logarithm? (3)

A

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
Q

Why do we use Q to describe frequency along the BM? (4)

A
  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
Q

What is a Spontaneous rate of an ANF? (3)

A

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
Q

What is the difference between the LOW and HIGH SR (Spontaneous Rates)?

A

In ANFs, lower group Neuro fibers have close to 0 spontaneous rate which means fire less easily if not High intensity sound

58
Q

What is the difference between groups of ANF synapse IHC at Modiolar side vs. Pillar side?

A

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
Q

What are the 3 functional differences of the mechanisms for spatial difference?

A

Shape, size of ribbons,
Ca channels related to vesicle release
Recycle for threshold

60
Q

What are the mechanisms for the spatial difference for noise damage? (3)

A

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
Q

What does this graph demonstrate?

A

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
Q

What are Saturated RLF?

A

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
Q

What does this graph demonstrate?

A

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
Q

What do these graphs demonstrate?

A

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
Q

What are the three methods to examine temporal pattern?

A

Post (or peri) stimulus Time Histogram (PSTH)

PRH—period histogram

Interspike interval histogram

66
Q

How does the PSTH work?

A

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
Q

What does the PSTH show in this situation?

A

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
Q

What is phase locking?

A

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
Q

What does this graph show?

A

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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