Review on Cochlear Physiology Flashcards
What is the BV pathway to the internal auditory artery?
Starts from Vertebral A. to Anterior inferior cerebellar to A.-Internal auditory A.-common cochlear A. main cochlear A.
Describe the spiral modiolus artery (5):
Modiolar blood bed (supplies to SGNs)
Radial A. to the lateral wall—stria vascularis and others
VSBM (vessels of basilar membrane) may supply Organ of Corti
Capillary network to Collecting vein to spiral modiolus vein-back to larger vessels
What are the 7 branches in the cochlea and their targets?
To corner between spiral ligament and RM (1)
To SV (2)
To spiral Prominence (3)
To Spiral ligament (4)
Spiral limbus (5)
VSBM +spiral lamina (6)
Spiral ganglion (7)
What is the contact and blood supply to the OC?
No direct contact or supplies of blood to organ of Corti
Which of the 7 branches provides nutrition to OC
VSBM
Describe the capillary beds in the lateral wall:
In stria vascularis and spiral ligament
Blood vessel in the spiral ligament takes the major portion of blood supply of the cochlea
What is the role of the thick vessels in the spiral ligament?
Thick vessels in spiral ligament provide short circuit, to adjust blood flow via stria vascularis
The separation between endolymph and perilymph is established by _____________
Tight Junction
High K and positive potential in endolymph is generated and maintained by ________________________
Stria Vascularis
Most energy consumption in cochleae is by__________________________
the organ of Corti
What can we compare perilymph with?
Comparing with CSF and blood serum (suggests barrier between CSF and Blood)
Where is the perilymph generated?
Origin from serum at supra-ligament, and limbus regions
What is the movement particularity of perilymph?
The movement of electrolytes is followed by water through filtering, water movement is passive, and Ions pass first
Perilymph communicates with the CSF through the____________________
Cochlear aqueduct
What is the location for the reabsorption of perilymph?
Below BM at medial and lateral ends
What is evidence that there is a barrier between the blood and perilymph?
- Tracer kinetics: the tracer takes time to get into perilymph from the blood
- Ion differences between the two compartments
- Specificity and competitive inhibition: the existence of a special transportation system
What is the composition of endolymph?
Composition high in potassium and low in sodium
Where does endolymph originate from?
Originates from perilymph, via Stria vascularis not directly from blood
In the endolymph, transportation of K produces an ___________________
K transportation an EP generation
What is the one-pump model?
We have Two-cells, marginal and intermedial cells (currently accepted theory)
What is the role, location, and potential of marginal cells?
Role of marginal cells, pump face scala medious, positive intracellular potential
What is the role of intermediate cells?
Provide a source of potassium that can go through the ion channels below
What are the ion channels involved in the one-pump model between intermediate and marginal cells?
KCNJ10, Na-2Cl-K co-transporter (Gene SLC12A2),
KCNQ1-KCNE1 marginal cell
What is the meaning and pathway of the standing current?
Current flow without sound
Stria vascularis- OC - ST - back to Stria Vascularis
What are the 2 recycling pathways of potassium?
HC-SC-fibrocytes-StV
HC-cortilymph-SC-fibrocytes-StV
What are the cells involved in potassium recycling? (2)
supporting cells, fibrocytes
What are the special structures involved in K pathway and recycling?
Gap junction HC-SC-fibrocytes-StV cells
What are the two important proteins in the cochlea that form the gap junction?
Cx26, Cx30
What is one of the main causes of Genetic hearing loss?
Loss GJB2/6 (Most important proteins forming the gap junction Cx26, Cx30)
What happens to hearing from a mutation of GJB2?
50% autosomal non-syndromic are mutations of GJB2 which cause recessive HL, profound at birth
Is k-recycling theory correct for the hearing loss by GJB mutation? (2)
Lack of solid evidence that potassium recycling is broken down after mutation
Many HL-associated mutations of Cx26 does not disrupt K recycling
What are the characteristics of Type l ANF?
% or numbers
Shapes
myelination
Targets
Innervation patterns and names of fibers
Functions
95%
Bipolar
Myelinated
IHC
Afferent SGN Inner Radial fibers convergent innervation
What are the characteristics of Type ll ANF?
% or numbers
Shapes
myelination
Targets
Innervation patterns and names of fibers
Functions
5%
Pseudomonopolar,
Unmyelinated
OHC
Afferent Outer spiral fibers
Less known functions
What are ribbon synapses and what are their functions?
Ribbons shape synapses in retina cells (horseshoes), and in IHCs (American football)
Long-lasting release/response is common for all ribbon synapses, distinguished from conventional synapses, and fast release/response which is special for ribbon synapses in cochleae
What are the molecular components of ribbon synapses? (5)
ribeye A+B, Bassoon, otoferlin, CaV1.3, piccolino
Which NT is thought to be the main player in ribbon synapse?
Glutamate
What are the four evidence that Glutamate is the main NT of ribbon synapses?
- Glutamate is an amino acid existing every cell, rich in vesicle
- Can be released from synapse, agonism can activate AP in AN
- AP can be blocked by a special blocker against AMPAR
- It is not fully understood how the released glu can be removed (1) by glial cell, and (2) by endocytosis
What are the 3 ANF categorizations?
Low, medium and high SR units
What are the 3 ANF categories distinguished by?
They are distinguished by numbers, synapse location/morphology, threshold, dynamic sensitivity to noise
What are the special characteristics of Low/Medium SR ANF units? (6)
High thresholds, spread
Synapse IHC at modiolar side
Small terminals large ribbons
Large dynamic range
Code signal at high SPL and in noise
sensitive to noise damage
What are the special characteristics of
High SR ANF units?
Low thresholds close to behavioral one
Synapse IHC at pillar sides
Large terminals small ribbons
Narrow dynamic range
Resistant to noise damage
What do the “Typical” rate-level functions look like? (3)
Narrow dynamic range and saturation
Seen from high SR fibers
Seen at a frequency around CF
What causes a compression/non-linearity of the “Typical” rate-level functions? (3)
Synaptic features
The active mechanism by OHCs
Not fully understood
What are the two ways of Frequency analysis?
Place Coding and Frequency Selectivity
In the place coding tuning curve, what is it based on?
Tuning curve (based upon spike rate): Sharper at high frequency
Why tuning curve is sharper at the 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.
- Therefore, the input signal must be much stronger to excite the fibers at this CF location up to their threshold
What is frequency selectivity defined by in frequency analysis? (2)
Defined by bandwidth
Defined by log, Q value
How do measure the bandwidth from the Tuning curve for frequency selectivity?
BW is measured 10 dB above the threshold at CF.
BW is inversely related to frequency selectivity. Larger the BM, poor Frequency selectivity
Larger the BW, lower the Qvalue
Lower the BW, better the the frequency Selectivity
What is the formula for Qvalues
Q10 dB = CF/bandwidth (BW) of TC
The higher the Q value, the better the frequency selectivity
There is better frequency at _____________________
High frequency region (when frequency by logarithm)
What does phase locking improve?
Phase locking improve frequency selectivity at low frequency region, high intensity
What do we know about how frequency discrimination is done at high f, high intensity?
Don’t know how frequency discrimination is done at high f, high intensity
What are the 4 ways to observe phase locking?
- PSTH: peristimulus histogram
- PRH: period histogram
- ISIH: inter-stimulus interval histogram
- Stimuli: simple tone, complex tone, amplitude modulation (AM)
What is the physiological basis for phase locking?
neurotransmitter release at certain phases (when HC depolarized)
How do we examine phase locking in research?
Phase locking is examined by adding responses of many sweeps
How do we see phase locking in the real?
synchrony across many fibers: volley principle
What do we see about phase locking in intensity coding? (2)
- Phase locking shows a lower threshold and larger dynamic range than spike rate coding
- Reserve better the spectrum peak at high sound level
What do we see about phase locking in frequency coding? (3)
- Phase locking shows periodicity (frequency feature) of low frequency signal
- Contribute to the frequency selectivity at high intensity in the low frequency region
- This mechanism does not exist for high-frequency signal at high intensity.
What do we see about phase locking in Temporal coding?
When using AM, phase locking can be done in a similar way as behavioral study observing TMTF (temporal modulation transfer function)
What are the differences between PL and temporal coding? (4)
- Onset latency
- Onset-sustained ratio (peak rate/sustained rate)
- Response to gap
- Response to forward masking (not detailed)
How is the dynamic range of hearing is established by AN?
The dynamic range (behavior dynamic range = change in Sound level cause loudness perception ) of human hearing is something around 120 dB.
In intensity coding, what is the distribution of thresholds like? (3) (Increase Dynamic Range by Threshold Distribution)
- Most fibers have thresholds within 20-40 dB above the absolute threshold
- Spread to 60-80 dB above abs threshold only for less than 10% of fibers.
- Nerve fibers with high thresholds often have low spontaneous spike rate and often receive efferent inhibition on their terminals with IHCs
At which part of the sound do we see a greater dynamic range?
Greater DR is seen at the onset of the sound
We measure at a long time window and count the total spikes
+ =shorter time window from onset peak we see high increase
Squares = if the time window is longer we see more saturation
In RLF comparison across different groups, we can see ______________ show ______________ saturation and __________ units show _____________ saturation
Higher SR, more significant saturation
Lower SR units, you see no saturation
What causes a Two-tone suppression seen in RTF?
Phenomenon from mechanical interaction due to two sounds, If we add a second tone, with an increase of the intensity of tone two, spike rates will decrease
Tone two is shown as the bar on top in the graphs to the left
In the mechanisms for coding intensity, what is the Spread of excitation?
BM vibration spreads to high-frequency areas at high intensities
More 8th N fibers will be accumulated to code intensity
Problems with this model:
Can’t explain broadband noise
Failed in exp using band rejected noise (if spreading works, response in notch noise should saturate quicker
Increase of sound level: the neurons around Cf may get saturated, however an increase in sound level will excite more surrounding neurons thus will be recruited and contribute to the spike rate
How can push up the working range?
By using background noise
Background noise shifts the working range of ANFs (push it up)
Q: quiet, all other curves having background noise as indicated by the number for the noise in spectrum level (in dB re 20 uPa/Hz)
C and D are normalized from A and B respectively
A and C: a high SR ANF
B and D: a low SR ANF
What is the effect of Background noise on Low SR ANFs and Low SR units? (4)
- highly resistant to noise (in terms of their response to signal)
- High SR units, saturated by background noise
- Low SR units are critical for signal coding in noise
- Low SR units are more sensitive to noise damage
How does intensity affect Phase locking?
Increased phase locking with intensity
Phase locking occurs before significant rate increase, so PL has lower threshold than rate threshold
What are descending pathways in the Corticofugal (centrifugal) innervation to ears?
Centrifugal innervation exerts top-down processing
Loop between auditory cortex (AC) and MGB
AC- IC-MOC
AC-MOC
IC-CN
Our focus: MOC N contralateral cross middle line .— back to cochlea
What are Ascending pathways in the Corticofugal (centrifugal) innervation to ears?
Ascending:
***PVCN-MOC
AVCN-IC-MOC (less clear)
DCN to SOC (?)
What is the location of the neurons in the cochlear efferent from the lower brainstem?
in perinuclei of SOC
What are the 2 groupings of the efferent neurons?
LOC n.->UOCB -> afferent terminals at IHC
Thin, unmyelinated
Mostly go to the ipsilateral (uncrossed) cochlea
Unknown function
MOC n ->COCB ->OHC bodies (lateral basal surface) More accessible, fibers are thicker and produce stronger AP and easier to be recorded
NT: ACh***
GABA
CGRP
Thick, myelinated fibers
Mostly go to contralateral (crossed) cochlea
However, the whole loop double-crosses the midline which causes a stronger ipsilateral effect
What are the whole loops of reflex? (2)
CN to ctrla. MSO and then crossed back
CN to ipis. LSO uncrossed and then uncrossed to ipsi. cochlea
Stimulating one ear results in efferent feedback to both ears
Describe the MOC physiology:
Davis battery theory
Current and resistance across OHCs
Resistors in parallel and in serial
What is the function of Ach on OHC? (3)
Increase opening of a special type of K channel (ligand gated)
Shunt effect: OHC leaking, reduced resistance
Larger K current via OHC in resting and response to sound
What can we see in vitro from the effect of Ach on the motility of OHC?
There is conflicting evidence because in vitro ACh reduces stiffness and increased body motility, but in vivo there is reduced OHC gain
What is the evidence of MOC acting on OHC?
Changes in IHC potential, CAP and OAE
What are the functional features in nature of how MOC acting OHC?
Frequency selectivity
Bilateral response to unilateral stimuli
How does MOC activation changes CAP?
amplitude reduction and threshold elevation
How does MOC activation affect IHC?
IHC receptor potential change
Changes of CAP amplitude and IHC potential from MOC activation are significant at ___________________________
Lower sound levels
What does the fact that the changes of CAP amplitude from MOC activation are significant at low sound levels suggest?
Suggesting the effect via OHCs
What are the evidence for MOCB, not LOCB?
The effect of shock rate suggests the role of MOCB
Peak shock rate at 300/s, only MOC can respond because the refractory period is longer for LOC
What are the important points of the MOC efferent acoustic reflex? (3)
- Double-crossing pathway
- Ipsilateral one is stronger
- The acoustically evoked reflex is weaker than the result of electrical stimulation of MOCB
Where do we do a suppression test for the MOC efferent acoustic reflex? (2)
- Easier to do in contralateral suppression
- Weaker effect
What have suppression studies shown us so far?
Mainly contralateral, by acoustic stimulation (natural activation of efferent
On OAE: non-invasive but too small (<3 dB)
On CAP: up to 10 dB, difficult to do
Unmasking on CAP and speech
Need more research and simplification
What is the role of the MOC efferent AR in hearing? (2)
- Protection against NIHL—minor roles
- Improve signal processing
Anti-masking effect
Adjust ANFs working (level) range according to listening environment
Gan control to enhance fluctuation profile
Attention selection
