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Audition II > Unit 2 - Lecture 3 > Flashcards

Unit 2 - Lecture 3 Flashcards

1
Q

Centrifugal innervation

A
  • Ascending vs. descending
  • Exerts top-down processing
  • Optimizes the encoding of ascending signal processing
  • Best investigated in the cochlear control by lower brainstem
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2
Q

Ascending and descending pathways are working together which optimizes the ____ of signal

A

Encoding

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3
Q

What is the major loop?

A

The major loop is from PVCN to MOC

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4
Q

What is the minor loop?

A

The minor loop is from DCN to LSO

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5
Q

The efferent neurons in SOC are located ____

A

Peripherally

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6
Q

Only the ____ is involved with the reflex

A

PVCN

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7
Q

The ascending projection mainly comes from the ____

A

PVCN

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8
Q

The descending from the ____ to cochlea

A

MOC

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9
Q

Descending projects (3 + our focus)

A

AC—MOC N—cochlea

AC—IC—MOC N—cochlea

AC—IC—CN and LL

Our focus: MOC N.—cochlea

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10
Q

Ascending project (3)

A

SGN—PVCN—MOC neurons

SGN-AVCN-IC-MOC (less clear)

SGN—DCN(?)—LOC neurons

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11
Q

Ascending projection (not for efferent loop)

A

Note the projection from AVCN to SOC

AVCN to SOC is the projection for ascending

Efferent control is from the PVCN

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12
Q

Cochlear efferent innervation from brainstem
- location
- grouping
- cross vs. Uncross
- targets

A

Location of efferent neurons: in perinuclei of SOC

Grouping: medial versus lateral

Cross versus uncross: related to accessibility

Targets: afferent terminals under IHCs versus OHC cell bodies

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13
Q

Where are the efferent neurons located?

A

Perinuclei of SOC (divided to MSO, LSO)

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14
Q

Anatomy of LOC

A

LOC n. –> UOCB –> afferent terminals at IHC

  • Thin, unmyelinated
  • Mostly go to ipsilateral (uncrossed) cochlea
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15
Q

Anatomy of MOC

A

MOC n –> COCB –> OHC bodies (lateral basal surface)

  • Thick, myelinated fibers
  • Mostly go to contralateral (crossed) cochlea
  • However, the whole loop double cross the midline.
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16
Q

Why we know more about MOCB function?

A
  • MOCB is more accessible (stimulation and recording at brainstem surface below cerebellum (4th ventricle)
  • MOCB fibers are thick and myelinated, producing stronger action potential, easier to be recorded.
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17
Q

Circuit of efferent acoustic reflex (EAR)
- major loop
- target
- function

A
  • EAR is part of acoustic reflex (AR), but not the same thing
  • EAR
    • major loop is Cochlea-PVCN-MOC-Cochlea
    • Target: OHCs
    • Function: motility and cochlear gain
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18
Q

Proportions of crossed and uncrossed (in cat)

A

MOC
- Crossed 26%
- Uncrossed 11%

LOC
- Uncrossed 48%
- Crossed 15%

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19
Q

Why is there stronger ipsilateral control of the MOC?

A

Stronger ipsilateral control because the whole loop has more fibers double crossing

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20
Q

EAR vs. AR

A
  • It takes a while for MOC response to reach its maximum
  • For EAR, it takes time to activate the system (if you play a sound it wont be immediately activated like AR)
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21
Q

LOC circuits

A
  • LOC efferent is more numerous
  • LOC efferent is more ipsilateral (from LOC to cochlea)
  • CN source for LOC efferent is not well known
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22
Q

From PVCN to MOC: for the feedback loop to ____

A

OHCs

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23
Q

Explain why the ipsilateral MOC is strongest

A
  • Strong innervation from PVCN to contralateral MOC neurons
  • Weak PVCN to ipsilateral MOC neurons
  • Since MOCB is mainly crossed, there is a double cross for ipsilateral MOCB
  • Therefore, contralateral MOC reflex is 1/3 as strong as the ipsilateral MOC reflex
  • The ipsilateral MOC reflex is the strongest because it crosses over twice (double cross)
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24
Q

Medial efferents are more contralateral (____ to the ipsilateral MOCB) - ratio

A

3:1

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25
Q

Efferent feedback to one cochlea can be initiated by acoustic stimuli to ____ ear

A

Either

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26
Q

Contralateral reflex of MOC is ____

A

Weaker

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27
Q

Efferent density along cochlea

A
  • Stronger innervation occurs in the middle frequencies (density is higher)
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28
Q

Tonotopic feature in the EAR loop (what is the point of efferent innervation)

A
  • The point of cochlear stimulation receives the feedback
  • The point of efferent innervation is to control the gain of the OHC, so wherever you stimulate will be affected
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29
Q

Efferent Innervation pattern IHCs vs OHCs

A

LOC synapses on afferent terminal of IHCs

MOC synapses on OHC bodies

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30
Q

MOC-OHC synapse
- what is it
- where is it located
- what does it result in

A

Synaptic cistern is inside the synapse between the efferent fibers and the OHC

Because of the synaptic cistern, one OHC can receive innervation from multiple neurons

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31
Q

Efferent transmitters for MOC

A

MOC (clear): acetylcholine (ACh)

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32
Q

Efferent transmitters for LOC

A

LOC (unclear):
- ACh—the major one, clear function
- Dopamine (DA): modulate input to SGns: protection against intense noise
- GABA
- Dynorphin

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33
Q

Neurotransmitters in MOC-OHC synapse:

A

ACh

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34
Q

MOC activation

A
  • Depress BM motion
  • Depress IHC receptor potential
  • Depress CAP

Even though we see depression of the the IHC RP, it only controls OHC motility

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35
Q

MOC potential mechanism

A
  • Not directly on IHCs
  • Control of OHC motility
  • Control of cochlear gain
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36
Q

MOC stimulation impact CAP

A
  • Amplitude reduction occurs at low level
  • Depression of CAP at lower sound levels
  • At high sound levels the curves overlap
  • This suggests the effect of OHC
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37
Q

The effect of shock rate suggests the role of ____

A

MOCB

38
Q

Explain shock rate and MOCB

A
  • Peak at 300/s, only MOC can respond because refractory period is longer for LOC
  • This is showing why the MOC is doing all this and not the LOC (the rate is supper high and an unmyelinated fiber would not be able to handle this)
39
Q

Efferent stimulation by electrical shocks
- what does it impact
- what does it suppress
- where are there large shifts

A
  • Impact IHC potential via OHCs
  • Suppresses CAP and RLFs of ANFs, large shifts at low sound level
40
Q

Evidence for the contribution from OHCs

A
  • MOC stimulation is effective
  • MOC innervates OHCs
  • The peak shock rate corresponding to refraction time of MOC f.
  • CAP shifts at low sound level (the range of OHC active amplification)
41
Q

Inhibition on high SR fibers

A
  • RLF is shifting to the right with SR
  • M and L is plateau depression
42
Q

____ shifting by efferent stimulation

A

Right

43
Q

Impact of efferent activation on the maximal firing rate (where is reduction seen)

A

-Reduction seen only in L/MSR ANFs, not in the high SR groups

44
Q

Inhibition on low SR fibers
- where does it occur
- what is it related to

A
  • Depression occurs at whole range
  • Probably related with LOC innervation
  • But not clear how because eliminating LOC decreases SR, instead of increasing it
45
Q

____ stimulation changes tuning curve

A

MOC

46
Q

How does MOC stimulation change tuning curve?

A

By elevating threshold, narrow frequency range

47
Q

Efferent effect on OHCs
- hyperpolarization
- MOC potential
- Increases ____ by…
- Decreases ____ by…

A
  • Hyperpolarization: induced by ACh as the result of more K channel opening
  • MOC potential: negative in SM and positive in OC
  • Increases CM amplitude (hyperpolarization & shunt effect)
  • Decrease in OHC motility indicated by the suppression of CAP and OAE
48
Q

Is it clear how ACh reduces OHC in vivo?

A

It is not clear how ACh reduces OHC motility in vivo, because the in vitro evidence suggests opposite.

49
Q

How do the OHCs effect endocochlear potential?

A
  • Another pathway is added by the medial cochlear efferent
  • With the extra pathway through the MOC, there is more current which causes a change in the EP (Reduced EP as there is more K in the scala media)
  • Modified Davis’ battery theory
  • Also called the shunt effect
  • There is also an increase in CM
50
Q

MOC activation decreases ____

A

OHC motility

51
Q

What does MOC stimulation cause?

A
  • MOC stimulation depresses DPOAE
  • MOC stimulation depresses CAP: more shift at low level which involves active mechanism
  • Suggesting reduced OHC motility
  • However, exact fact and mechanism are unclear
52
Q

DPOAE comes from ____

A

OHC motility

53
Q

ACh effect on OHCs

A
  • Increases conductance, MET current
  • Reduce stiffness
  • Increase motility (in vitro)
54
Q

Why is ACh on OHC motility contradictory to in vivo data?

A
  • CAP OAE suppression
  • Reduction in BM motion
55
Q

How does MOC on OHC reduce active part of BM motion?

A
  • Not fully understood
  • The CM increase due to shunt effect
  • In vitro studies show reduced stiffness and increased motility of OHCs.
  • Big contradiction with the depression of CAP, IHC receptor potential, OAEs, all pointing to a reduction in OHC motility
56
Q

MOC on TEOAE

A

If MOC is stimulated, the OHC motility is reduced by the reduction of the TEOAE

57
Q

Efferent on SOAE
- ____ is used to evoke efferent effect
- what do we need to rule out?

A
  • Controversial issue
  • Lack of animal data
  • In human, contralateral stimulation is used to evoke efferent effect.
  • However, need to rule out the role of acoustic reflex via middle ear
58
Q

Efferent control reduces cochlear gain which is largest at ____ sound levels

A

Lower

59
Q

Cochlear gain by OHC is larger at ____ sound levels and the depression is also ____ at lower sound levels

A

Lower, Larger

60
Q

Cochlear gain compression

A
  • Compression is the nonlinearity of the cochlear gain (gain is reduced at high level)
  • Increases at low sound levels and saturates at high sound levels
  • Close to CF, active mechanism is level dependent
61
Q

Compression in animals

A

In animals, gain can be derived by the rate-level functions of either BM vibration or neural spike rate.

62
Q

Compression in humans

A

In humans, behavioural measures must be used, mostly based upon forward masking

63
Q

Test cochlear compression by forward masking in humans

A
  • Masker (rather than signal) level as the dependent variable
  • Compare off-fre and on-fre masking at any level.
  • The gain is the difference between these
64
Q

What masking do you use to test compression?

A

Forward masking

65
Q

What is gain?

A

Gain = the difference between on and off masking

66
Q

Compression is shown as the ____ gain at higher sound level

A

Reduced

67
Q

The result of forward masking in humans (where is there a larger difference)

A
  • Larger difference at lower sound levels
68
Q

The feature of OHC amplification

A
  • Frequency selective
  • Level selective (highly compressive)
69
Q

Going to have more gain at ____ sound levels

A

Lower

70
Q

What is the unmasking effect?

A

The threshold that you need to hear becomes lower

71
Q

When using the unmasking effect of cochlear efferent, what SR groups is this seen in?
- tone bursts vs. Continuous noise

A
  • Seen in all SR groups, more for low SR units
  • When you have tone bursts in quiet with MOC activation there is a shift to the right
  • When continuous noise it shifts to the right and plateau depression
72
Q

LOC functions

A
  • On the excitability of the afferent ANFs
  • Protection on afferent IHC-SGN synapses
  • 84 dB SPL noise 168 hours show no synapse loss in control mice mice but 40% loss in mice with deefferentation surgery (Got rid of LOC efferent and saw this effect (40% loss of control))
73
Q

Other effects of LOC

A
  • At high intensity: provides 20-30 dB attenuation, especially for low SR fibers, protect afferent synapses (IHC-SGN)
  • Suppression of cochlear responses via Acoustic Reflex to the cochlea (not ME)
74
Q

Activation cochlear efferents by electrical stimulation

A
  • Activation cochlear efferents by electrical stimulation is not natural, the result is much stronger than what can be reached in real hearing
  • EAR can be evaluated by natural activation of the circuit: acoustic stimulation
  • Suppression of OAE, CAP
  • Masking release in CAP, and speech
75
Q

How to see the fre selective depression?
- how is DPOAE evoked?
- what depresses DPOAE?
- how is frequency selectivity examined?
- where does the largest depression occur?

A
  • DPOAE is evoked by two tones of f1 and f2 at the test ear.
  • Contralateral stimulation depresses DPOAE.
  • The frequency selectivity is examined by changing the frequency of contralateral signal
  • The largest depression occurs at the region of f1 and f2
76
Q

Evaluation 1 - What happens with suppression of OAE?
- variable up to ____
- what can be used and when?
- what are contralateral suppression signals?

A
  • Suppression variable up to 3 dB
  • Both TEOAE and DPOAE can be used, but TEOAE is better for low frequency and DPOAE for high frequency
  • Contralateral suppression signals: noise or tones at or below moderate level (avoid saturation and AR through middle ear)
77
Q

Evaluation 2 - What happens with suppression of CAP?
- how to record CAP
- how is it reduced

A
  • Record CAP in ECochG
  • CAP amplitude reduced by contralateral signal
  • Larger reduction (up to 10 dB)
  • Frequency selective
78
Q

Ipsilateral MOC suppression on DPOAE - suppression is indicated by ____

A

Adaption

79
Q

DPOAE suppression by contralateral signal (CS)
- when does the adaptation occur?
- how long until plateau?
- what is the overall magnitude of suppression?

A
  • The adaptation after onset
  • Long latency for suppression to reach plateau (2-3 min)
  • Overall magnitude of suppression < 3 dB
80
Q

Contralateral suppression on CAP

A
  • Larger suppression at low sound level
  • Larger suppression in CAP than DPOAE (10 dB in CAP versus 3 dB in DPOAE)
81
Q

Evaluation 3 - masking release in CAP

A
  • Measure masked CAP
  • Apply contralateral signal
  • CAP improved
82
Q

Evaluation 3 - masking release in speech perception in noise
- where does the noise and speech go?
- what improves speech perception?
- what must the noise be?

A
  • SNR for speech perception performance (noise and speech to one ear)
  • Contralateral noise: speech perception improves
  • Must be independent noise
83
Q

Why might speech reception with contralateral noise improve?

A

When you have a masked CAP and add contralateral signal, CAP improves

84
Q

Masking release on speech perception - conflictions

A
  • Conflicted results are reported
  • No animal data
  • Difficult in the test control in clinic
85
Q

The role of efferent control in hearing (2)

A
  • Protection against NIHL (may not be the major role)
  • Improve signal processing
86
Q

Protection against NIHL

A
  • Efferent inhibition reduced ANF firing rate
  • MOC activation (enhancement) decreases NIHL
  • MOC de-efferentation increases NIHL (by lesion, by blocker perfusion)
  • Both MOC and LOC provides protection against noise induced synaptic loss
  • Negative reports also available
  • Efferent modulates cochlear gain by only 20 dB, mostly at low sound level
87
Q

Conflicting results exist on NIHL defined as ____ shift

A

Threshold

88
Q

Protection against NIHL is varied by the features of ____

A

Noise exposure

89
Q

The protection on noise induced synapse loss appears to be ____

A

Consistent

90
Q

Anti-masking effect of EAR

A

Add contralateral suppression, the response gets better

91
Q

Large fluctuations are formant ____, small fluctuation at format ____

A

Trough, peaks

92
Q

Role of efferent in signal processing

A
  • Anti-masking effect by MOC
  • Reset the ANFs to work in different level range
  • Gain control enhance the fluctuation profile
  • Attention selection

Audition II (7 decks)

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