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HESP 653: Anatomy and Physiology > Final Review Q&A > Flashcards

Final Review Q&A Flashcards

1
Q
  1. What are the 2 main functional purposes of the pinna?
A
  1. Filters acoustic input (amplifies and dampens various sounds)
  2. Vertical plane sound localization
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2
Q
  1. What are the major audiological consequences of pinna damage?
A

none; only minor damages.

trouble wearing a BTE HA

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3
Q
  1. The children the ear canal is roughly what direction? In adults?
A

Children: mostly perpendicular to
Adults: roughly perpendicular, but slightly downward at the end (helps avoid water collection)

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4
Q
  1. What is the general shape of the ear canal? What is it shaped like this?
A

“lazy S-shaped”;
-pars externa= inward, forward, and upward
-pars media= inward and backward
-pars interna= inward, forward, and downward
curvy nature of EC provides protection against puncturing the TM.

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5
Q
  1. What portion of the ear canal is surrounded by cartilage? Bone?
A

Cartilage: lateral 1/3 of EC (dynamic glands and hairs)
Bone: other 2/3 of EC (fixed size and skin tight lining)
-bony portion not fully formed in kids until 3 so be careful, can affect immittance measurements

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6
Q
  1. Cerumen is produced in what part of the ear canal?
A

the lateral 1/3 of the EC

-cerumen: subacious glands (oily-lubrication) + ceruminous glands (waxy)

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7
Q
  1. What is the function of cerumen?
A

lubrication

protection (antibacterial, anti-fungal, and anti-insectual properties)

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8
Q
  1. The ear canal primarily acts like what kind of resonator?
A

an open-closed pipe resonator. The closed end is not completely reflective, causing the peaks in the output response to be broadly tuned.

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9
Q
  1. At what frequency is the primary resonance of the ear canal and meatus?
A

2.5 kHz

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10
Q
  1. What parts of the body contribute to the resonances by the time one reaches the tympanic membrane?
A
  • head
  • neck, torso, etc.
  • concha
  • pinna
  • EC and TM

generally, there is a boost from 2-7kHz

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11
Q
  1. What portion of the Eustachian tube is surrounded by cartilage? bone?
A

Bone: superior 1/3 portion
Cartilage: inferior 2/3 portion
*at rest, cartilage portion is closed and during action opens b/c of 2 muscles, levator veli palatini and tensor veli palatini.

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12
Q
  1. What nerve runs next to the middle ear cavity?
A

The facial nerve (CN VII)

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13
Q
  1. What is the promontory? What is its function?
A

“big bump” that is the basal turn of the cochlea.

Function: protects both windows by being the first contact point of objects through the middle ear.

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14
Q
  1. What vein runs next to the inferior wall of the middle ear cavity? What type of tumor is common to destroy this wall?
A

jugular vein

glomus jugulare tumor

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15
Q
  1. The children the Eustachian tube is roughly at what angle? In adults?
A

Children: almost horizontal
Adults: downwards at a 45 degree angel

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16
Q
  1. What are the names of the ossicles?
A

Malleus (hammer), Incus (anvil), and Stapes (stirrup)

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17
Q
  1. The middle ear bones solves what major problem in the transduction of sound?
A

The impedance mismatch of going from the large surface area of the TM to the small surface area of the oval window.

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18
Q
  1. What are the three mechanisms that the ossicles improve sound transduction?
A
  1. change in surface area
  2. lever action- acting like a tetter totter (2 arms; one longer than other)
  3. buckling of the TM
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19
Q
  1. The tympanic membrane moves in what direction?
A

Inward toward the ME in a buckling motion.

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20
Q
  1. Which of the ossicles is the weakest and most likely to break?
A

Incus- at its long process specifically.

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21
Q
  1. The cochlea is house where?
A

In the temporal bone

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22
Q
  1. What boney element surrounds the cochlea?
A

The otic capsule, the skeletal element enclosing the inner ear mechanism

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23
Q
  1. What are the types of temporal bone fractures? How often do they each occur? Which is worse?
A

Types: longitudinal (70%) and transverse (30%).
How: Longitudinal TB fractures occur because of severe head injuries. Cause: SN, C HL, Balance problems, and facial nerve damage/paralysis (20%). Transverse fractures occur because of fractures through the otic capsule and internal auditory meatus (IAM). Cause: profound SNHL, severe vertigo, and facial nerve damage/paralysis (50%).
Transverse fractures are worse.

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24
Q
  1. The cochlear has how many turns?
A

2.5 (2.2-2.9) turns— turns are smaller at apex than at base

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25
Q
  1. How long is the average cochlea?
A

33mm long

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26
Q
  1. The central axis of the cochlea is called what?
A

Modiolus- holds up the cochlea duct; has perforated bony core and accommodate nerve fibers.

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27
Q
  1. What is the function of the spiral lamina?
A

Shelf like structure that wraps around the modiolus from base to apex that connects the outer wall at the spiral ligament. AN fibers pass between this structure. Separates duct into 2 passages with scala media.

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28
Q
  1. What are the two windows of the cochlea? Where are they located (which is superior)? What is
    attached to them?
A

Oval and Round windows. Both are located on the cochlea. The oval window is superior. Stapes is connected to the oval window, which is the attached to the scala vestibuli. The round window is inferior to the oval window and is attached to the scala tympani. This membrane keeps the cochlear fluid in the cochlea.

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29
Q
  1. What are the 3 scala and where are they located?
A

scala vestibuli, scala media (or cochlear duct), and scala tympani. They are all located within the cochlea. The scala vestibuli is the most superior and the scala tympani is inferior. The scala vestibuli and scala tympani communicate at the helicotrema. The scala media is between the other scala and is separated by the basilar membrane and Reissner’s membrane.

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30
Q
  1. What divides the 3 scala and where are they located?
A

Reissner’s and basilar membrane. Reissner’s membrane is superior in that it is the floor of the scala vestibuli; separates endolymph and perilymph. basilar membrane is inferior and makes up the floor of the scala media/ the ceiling of the scala tympani. (wording??)

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31
Q
  1. Describe the size and stiffness of the basilar membrane.
A

at the base: narrow (.04mm), thin, and stiff.

at apex: wide (.36mm), thick, and floppy/flexible

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32
Q
  1. What is the main organ of hearing?
A

The organ of corti– within it are the HCs

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33
Q
  1. What gelatinous flap of collagen lies above the organ of corti?
A

Tectorial membrane- has notches on underside to accommodate tallest OHC allow the membrane to vibrate w/o decoupling

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34
Q
  1. What is the purpose of the stria vascularis?
A

-battery for the system Davis battery theory
-secretory and absorptive function of the blood supply.
-produces endolymph
-provides oxygen for basic metabolic control of the cochlea .
The cells in the sria vascularis maintains the +80mV ion charge of the endolymph.
—high K+ ions and low Na+ ions

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35
Q
  1. What are the two types of hair cells? What are their shapes? How many are there of each?
A

Types: Outer and Inner
Shape: O=test tubed shaped; I= falsk shaped
How many: Outer=3-5 rows (12,000 cells) , Inner=1 row (3,500 cells)

*divided by a tunnel and held in place by supporting cells.

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36
Q

38.What shape are the two types of hair cells arranged?

A

OHC: stereocilia form a “W” shape
IHC: stereocilla from a continuous “U” shape

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37
Q
  1. Which of the hair cells have contractile proteins? Why do they have them?
A

OHC.
Why? allows for contraction and expansion that are active during depolarization (contracting) and hyperpolarization (expanding)

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38
Q
  1. Which hair cells are the main transducers of sound?
A

IHC

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39
Q
  1. In what direction does a rarefaction deflect the basilar membrane?
A

upwards—> causes shearing of the sterocillia

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40
Q
  1. In what direction does a rarefaction open the ion channels at the end of the stereocilia?
A

laterally/ away from the limbus–> depolarization (excitation)

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41
Q
  1. Tip links do what for stereocilia?
A

mechanically open/close the ion channels

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42
Q
  1. Why does the traveling wave goes from base to apex?
A

Starts at the mass/stiffness dominated portion (the narrow, thick base) —> travels to the

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43
Q
  1. The tuning on the basilar membrane is improved by what?
A

the cochlear amplifier adding mechanical feedback energy to the TW

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44
Q
  1. How does the basilar membrane tuning of a zombie compare to an alive person?
A

Zombie: more broadly tuned and requires greater input intensities –> broader TC w/ higher thresholds
everything becomes linear
Human: maximal peak displacement is achieved at lower intensities and sharper tuning at the CF

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45
Q
  1. How does the sensitivity of a zombie compare to an alive person?
  2. how long does the TW take to go from base to apex in a human.
A

zomebies: reduced sensitivity–> higher thresholds

48. 10ms

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46
Q
  1. How does the tuning at the basilar membrane change with level?
A

broader at higher intensities and sharper at lower intensities.

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47
Q
  1. What are on the axes of a tuning curve?
A 
X= frequency
Y= amp of BM vibration
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48
Q
  1. What frequencies show linear basilar membrane input-output functions?
A

those far from the CF; “off frequency”

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49
Q
  1. Why were von Bekesy’s original Nobel prize winning measurements questioned?
A
  • used cadavers (a problem if tuning is metabolic dependent (which it is))
  • used extremely high intensities
  • examined cochleas were damaged
  • tuning was too broad to identify freq. selectivity
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50
Q
  1. Why were von Bekesy’s original Nobel prize winning measurements questioned?
A
  • used cadavers (a problem if tuning is metabolic dependent (which it is))
  • used extremely high intensities
  • examined cochleas were damaged
  • tuning was too broad to identify freq. selectivity
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51
Q
  1. How does the tuning curve of a hearing impaired person compared to a typical hearing person?
A

NH: sharp TC and low intensities
HI: broad TC and higher intensities –> active feedback mechanism from the cochlear amplifier is impaired. increase in intensity–> broader peak displacement on BM and more acoustic compression–> broader curve.

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52
Q
  1. Does the amplitude of the traveling wave grow or diminish as it travels down the cochlear duct? Why?
A

grows b/c less stiff at apex making it more springy–> same force at base will create greater amplitudes at apex.

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53
Q
  1. After reaching the resonance point, how fast does the traveling wave dissipate? Why?
A

Very quickly; almost immediately. after resonance point, moves into the mass limited system reducing the TW’s amplitude.

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54
Q
  1. Scala media is filled with what kind of liquid? What is the voltage of the liquid?
A

Endolymph.–> poistive endocochlear potential = critical for normal cochlear function
positive (+80mV); high K+ and low Na+ ions)

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55
Q
  1. Scala vestibuli is filled with what kind of liquid? What is the voltage of the liquid?
A

Perilymph

near ground potential (high Na+ and low K+ ions)

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56
Q
  1. Scala tymapni is filled with what kind of liquid? What is the voltage of the liquid?
A

Perilymph

near ground potential (high Na+ and low K+ ions)

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57
Q
  1. What is the resting voltage of the outer and inner hair cells?
A

inner: -45mV
outer: -70 mV

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58
Q
  1. Why is it important to have a potential difference across scala media and hair cells?
A

to allow a flow of ions between the scala media and the hair cells–> allowing for depolarization and hyper polarization of the hair cells which is need for transduction, which is need for convert sound into neural activity.

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59
Q
  1. What is the source of the endocochlear potential? What types of cells help generate it?
A

positively charged endolymph.

OHCs

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60
Q
  1. Where are the ion channels on the stereocilia?
A

near the tips of the stereocilia

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61
Q
  1. Stereocilia must be fast enough to do what?
A

“faithfully reproduce high-freq. acoustic signals”

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62
Q
  1. What are the cochlear potentials? Which respond to stimuli?
A 
Resting:
-endocochlear potential
-intracellular potential 
Active: 
-cochlear microphonic
-summating potential 
-compound action potential

Active respond to stimuli (acoustic info causes a change in electric current).

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63
Q
  1. Which potential mimics the stimulus fine structure? Is it more like AC or DC?
A

Cochlear microphonic– AC
which also is a reflection of the stereocillia
like the diaphragm of a mic–> catches the vibration of the stimulus

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64
Q
  1. Which potential mimics the stimulus envelope? Is it more like AC or DC?
A

summating potential– DC

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65
Q
  1. Where is the compound action potential generated?
A

Spiral ganglia although it can be measured in the cochlea.

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66
Q
  1. What goes up to higher frequencies, the cochlear microphonic or the inner hair cell potential?
A

CM, although the inner hair cells resemble the CM.

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67
Q
  1. What cells produce OAEs?
A

OHC

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68
Q
  1. What houses the insides of a cell?
A

the lipid bilayer known as the plasma membrane

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69
Q
  1. What is the purpose of the proteins in this housing?
A

link between inter- and extra-cellular worlds

  • stabilize the membrane
  • transport ions and molecules
  • anchoring membrane to adjacent cells and substrates
  • cellular motility
  • communication
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70
Q
  1. How does a cell nucleus transport peptides or lipids?
A

through the golgi complex.

71
Q
  1. What do mitochondria do?
A

breaks down molecules to make energy in the form of ATP.

72
Q
  1. What is a neuron?
A

nerve cell; the basic building block of the nervous system.

responsible for communication info re: internal environment

73
Q
  1. What are the 4 zones of a neuron?
A
  • input zone (dendrites- where chemical or electrical input is received)
  • action zone (soma-input is summed into all or nothing action potential)
  • transmission zone (axon-myelinated pathway w/ breaks in pathway (nodes of rainvier) carries the electrical info to the telodendria. it jumps quickly from node to node)
  • output zone (telodendria- long strands of neural tissue w/ terminal boutons at end, which are packed with neurotranmitters.)
74
Q
  1. An increase in discharge probability is what kind of input? Decrease?
A

increase= excitatory

decrease=inhibitory

75
Q
  1. Axons are covered in what? Why?
A

myelin sheath- fatty, insulating covering that prevent diffusion of ions across cell walls.

76
Q
  1. What is a synapse?
A

connection between neurons.

3 types: axodendritic, axosomatic, axoaxonic

77
Q
  1. How do the short lived mini-potentials generate an action potential?
A

these mini potentials can be inhibitory postsynaptic potentials (IPSPs) or excitatory postsynaptic potentials (EPSPs). These mini potentials (attach to the dendrites or soma) combine their voltages to determine whether the neuron will achieve the necessary voltage to generate an action potential.

78
Q
  1. Describe the voltage and transfer of chemicals in an action potential.
A
  • The neuron (or HC) that has the potential to generate an action potential.
  • At rest, there is negative resting potential b/c of ion pumps.
  • After the summation of IPSPs and EPSPs cause enough depolarization to reach the action potential, the neuron spikes (fires-AP travels down the axon to the terminal boutons) because of the rapid influx of positive ions (ex. K+).
  • the neuron then begins to to return to resting state by hyper polarizing, causing the charge to first dip below the resting potential then recover/return to homeostasis.
79
Q
  1. How many sections of the 8th nerve are there? What are the sections? What is the mnemonic that helps remember which part section is above the other?
A

4: Facial nerve, cochlear nerve, superior vestibular nerve, and inferior vestibular nerve
7-up, Coc-down, SVN, IVN

80
Q
  1. What is the anatomical pathway that the auditory nerve fibers are attached to the hair cells?
A

wrapped around the trunk of the modiolus–>Spiral ganglia–> Rosenthal’s canal–> spiral lamina–> holes in spiral lamina (habenula perforata)–> unmyelinated fibers leading to the terminal boutons, which are attach to the HCs

81
Q
  1. What is a ganglion?
A

cluster of neurons that are located outside of the central nervous system (i.e. in the periphery)

82
Q
  1. What is the auditory nerve innervation density as a function of frequency?
A

Base and apex= 400/mm fibers (3-4/ IHC)

1-2 kHz= 1400/mm (15/IHC)

83
Q
  1. How many auditory nerve fibers are there in a human
A

30,000

84
Q
  1. What percentage of AN fibers are type I?
A

Type I: radial

90-95%

85
Q
  1. What type of connections do type I AN fibers have? Type II?
A 
Type I (radial) : IHC only in many fibers-to-one cell fashion
Type II (longitudinal or spiral): OHC only in one fiber to many cells
86
Q
  1. What AN fibers surely encode sound?
A

IHC- so type I (radial) fibers.

87
Q
  1. Where do the afferent and efferent AN fibers connect to IHCs? OHCs?
A

IHC: afferent- directly; efferent-indirectly (on afferent fiber)
OHC: afferent and efferent=directly.

88
Q
  1. Describe the tonotopic organization of the auditory nerve.
A

Base of the twisted AN =HF and apex=LF; mirror the tonotopic organization of the cochlea.

89
Q
  1. What type of fibers do we know a lot about and why?
A

Type I fibers.

Why? hard to find and record type II

90
Q
  1. Most neurophysiological information about the auditory system is conducted in what kind of experiment? What is measured in these experiments?
A

single cell neurophysiology experiments

measures changes in spikes (firing) rate of individual neurons when play a stimulus multiple times

91
Q
  1. How is a PSTH generated?
A

make time intervals (bins) and record the number of responses (number of spikes) that occur within that bin. for the duration of

92
Q
  1. How is a period histogram generated?
A
  • number of spikes are recorded after the completion of one period.
  • number of spikes recorded in time, but the x-axis resets every period.
  • -so stimulus is only played for one period and the amount of firing that occurs within that period is recorded.
93
Q
  1. How is an interspike interval histogram generated?
A

number of spikes recorded in time, but the timer is reset after every spike.
the duration between spikes is noted for which bin the spike will fit.

94
Q
  1. Describe the main sections of a primary-like PSTH? Why is it called primary-like?
A

spontaneous firing, onset, steady state, recovery

why? they are the most simple; it’s the first encoding o f the sound– no major transfers in sound info.

95
Q
  1. How does a PSTH get converted to a tuning curve? Response area?
A

TC: using the spont rate thresholds to plot the neural threshold(y-axis) as a function of frequency (x axis).
draw horizontal line

Response area: look at the steady state of a PSTH and pick a stimulus level, and plot neural firing threshold (spikes/sec) as a function of frequency.
draw vertical line

96
Q
  1. Describe the shape of low- and high-frequency tuning curves.
A

LF CFs: broader and symmetrical

HF CFs: sharper and asymmertical

97
Q

99.What is the measure of sharpness of a tuning curve? How is it calculated? Is a higher number sharper or broader?

A

Q10 value- way to normalize CF as a function of freq
Q10=CF/BW. BW is determined to be the distance between the cure 10 dB above the CF point/threshold
Yes, a higher Q10 is sharper. lower is broader

98
Q
  1. Do low-frequency AN fibers have absolutely large tuning? Relatively large?
A

proportional speaking (so in terms of Q10), relatively large tuning.

99
Q
  1. At what spike rates do you subdivide thresholds for ANFs?
A

<2 spikes/sec

100
Q
  1. What percentage of ANFs are within 10 dB of absolute threshold?
A

70%

101
Q
  1. Describe the relationship between spontaneous rate and threshold for ANFs.
A

Low spont rate= high thresholds—> need more to get them to fire
high spont rate=low thresholds (to voltage change to cause excitation; easily excitable)–> need less to get them to fire.

102
Q
  1. What is phase locking?
A

time locking of neural discharges to the acoustic wave form.

103
Q
  1. What is the limit of phase locking for the auditory nerve?
A

most, up to 800 Hz, some up to 5 kHz

mostly related to refractory period, but HF phase lock for refractory and compressive periods.

104
Q
  1. What is the rate limit for firing for the auditory nerve?
A

5 kZ; HF (>5 KHz neuron fires with equal probability at every part of the cycle of the input)
(<5 kHz ANF fires with the equal probability at a particular phase.; each fiber may not fire on every cycle as seen in the high freq).

105
Q
  1. Why does the AN only fire in a preferred cycle/phase in response to a sine tone?
A

excitatory (depolarization) happens in 1/2 cycle/ phase while inhibition (hyperpolarization) happens in the other.

106
Q
  1. Why does the response of an ANF to a click have multiple peaks?
A

ringing.

107
Q
  1. Why does the duration of the response of an ANF to a click get shorter with increasing CF?
A

rarefaction open the ion channels and the

108
Q
  1. Does the ANF respond at the rate of the input or at the intrinsic rate of the neuron?
A

input

109
Q
  1. How is the characteristic frequency determined for an ANF?
A

greatest peak/# of spike

110
Q
  1. What limits the phase locking of an ANF?
A

freq. b/c phase locking decreases with increasing freq

111
Q
  1. What is the dynamic range problem for the AN?
A

the preceptual DR for humans is larger (120-140 dB) than the neuron’s DR (20-50 dB) so how can we encode the full perceptual DR fit within the neuron’s DR.

112
Q
  1. How is the dynamic range problem solved?
A

there are multiple neurons w/ diff spont rates and they encode diff regions

113
Q
  1. Since compression occurs, what might help us encode/perceive vowels?
A

synchronization as a function of level is still reflective of the formant peaks although compression compromises the rate of firing at high intensities.

114
Q
  1. What does this suggest about the range of useful formant frequencies?
A

that the useful limits for vowel formants are 500 hz or below, (less than 4 kHz)

115
Q
  1. Describe the difference between suppression and inhibition?
A

suppression is a part of the BM mechanics, inhibition is a chemical process

116
Q
  1. What is one possible cause of two-tone suppression?
A

related to non-linearity of the BM

117
Q
  1. How do you measure the suppressive sidebands of an ANF tuning curve?
A

by reducing the firing rate by 20%

118
Q
  1. Describe the general shape of the response of an ANF nerve fiber to a narrowband noise as a function of bandwidth?
A

the spectral height is the same by an increase in BW; energy is added outside the TC???
increase the BQ get more firing
increase level get more firing
at certain point get interaction and between diff areas on BM and that interaction causes diminished amplitude at the CF

119
Q
  1. Are all ANFs excitatory? Are any inhibitory?
A

excitatory

no

120
Q
  1. What is the “typical” DR of an ANF?
A

20-50 dB

121
Q
  1. Briefly explain the volley principle of phase locking.
A

some neurons will fire for some cycles, while other will fire for the remaining cycles. The firing between these sets of neurons will sum to represent the signal.

122
Q
  1. Briefly explain how lower than CF input frequencies might produce the largest firing rates of an ANF.
A
  • b/c the amplitude of low freq tones given the nature of the BM
  • off freq have linear responses, leading to greater firing rates.
123
Q
  1. How many sections does the CN have? What are they?
A

3: anterior ventral CN (AVCN), posterior ventral CN (PVCN), and the dorsal CN (DCN).

124
Q
  1. How is the CN tonotopically organized?
A

from low (AVCN) to high freq (DCN)

125
Q
  1. What are the 5 main cell types in the CN?
A
  1. spherical bushy cells
  2. stellate cells
  3. globular bushy cells
  4. octopus cells
  5. fusiform cells
126
Q
  1. What are the 5 main PSTH types in the CN?
A
  1. primary like (in the AVCN)
  2. chopper (AVCN)
  3. primary w/ notch (AVCN)
  4. onset (PVCN)
  5. pauser then buildup
127
Q
  1. Compared to the AN, the CN has this type of phase locking.
A

good phase locking in the CN (up to about 4000)
similar to AN
can vary by cell- AVCN has best cells for phase locking

128
Q
  1. Where are the spherical and globular bushy cells? Where do they project? They effectively act as what?
A
  • AVCN
  • project to bilateral SOC via the ventral acoustic stria.
  • predominately projects to the contralateral pathway
129
Q
  1. Inhibition changes PSTHs. It also changes rate-level functions. What is one change that can occur for a rate-level function when there is inhibition as compared to when there is none.
A

-creates non-monotonic rate-level functions

130
Q
  1. Which area has the best temporal processing in the CN? Spectral processing?
A

temporal: AVCN
spectral: DCN

131
Q
  1. What is the largest outflow from the CN?
A

ventral acoustic stria (longest w/ most projections) going to the SOC

132
Q
  1. What does the MSO do? What are the main inputs? What type of cell is it (EE, EI, EO, etc)?
A
  • medial superior olivary complex=MSO, disk shapes
  • computing Interaural time differences (ITDs).
  • Main inputs: primarily excitatory input!!! (ipsilateral, bilateral excitatory input from spherical bushy cells and contralateral, bilateral inhibitory input cells from globular bushy cells.)
  • EE cells tuned to frequency.
133
Q
  1. What does the LSO do? What are the main inputs? What type of cell is it (EE, EI, EO, etc)?
A

Lateral superior olivary complex (LSO), disk shaped
-computing interaural level differences (ILD)
-Main inputs: ipsilateral, bilateral excitatory input from spherical bushy cells and contralateral, bilateral inhibitory input cells from globular bushy cells.
mostly EI cells

134
Q
  1. Explain the tonotopic organization of the MSO.
A

over representation of LF (neurons for <4 kHz )– good or computing ITDs

** no reason to have HF neurons here since computes ITDs, which are at LF

135
Q
  1. Explain the tonotopic organization of the LSO.
A

over representation of HF— good for ILDs; they naturally exist at HFs

** no reason to have LF neurons here since computes ILDs, which are at HF

136
Q
  1. Are MSO neurons tuned to ITD or IPD? Why?
A

ITD; b/c phase varies by frequency????

137
Q
  1. Rank order the following in terms of firing rate at relatively large levels for an MSO neuron: ipsilateral, contralateral, bilateral.
A

(from most firing to least) binaural, contra, ipsi

**MSO is most strongly driven by contra input, but it is a binaural neuron

138
Q
  1. Draw firing rate as a function of ITD for the MSO.
A

see HW 9

139
Q
  1. Draw firing rate as a function of ILD for the LSO.
A

see HW 9

140
Q
  1. What is the major nucleus between the SOC and IC? Is it obligatory? What nucleus is it physiologically similar to?
A 
Lateral lemniscus (LL)
no, b/c CN connects directly to the IC and can bypass LL
similar to the inferior colliculus
141
Q
  1. What is the purpose of ICC? ICX? ICD?
A

ICC: receives primarly auditory input; exciatory input from contra CN, LSO, and ipis MSO. inhibitory from ipsi LSO and NLL
ICX: important for multi sensory input
ICD:receives descending input from the auditory cortex. projects in ICC

142
Q
  1. Explain the tonotopicity of the IC.
A

tuned from low to high in the lamina which correlate to the iso frequency sheets. ??

143
Q
  1. How do TCs in ICC compare to AN? ICD vs AN?
A

ICC: sharper (higher Q10) than the AN (b/c inhibition?)
ICD: multi-peak and broad (stellate cells cross multiple lamina)

144
Q
  1. List three stimulus properties that we start to get tuning to at the level of the IC.
A

Temporal characteristics: duration, rise-fall time, modulation rate (AM or FM), FM/AM sweep direction

  • IC neurons have a preference to modulation rate
    • getting more specialized neurons.
145
Q
  1. What is the limit of phase locking in the IC?
A

up to 600 Hz.

146
Q
  1. What are the three main sections of the MGB? Which is the main auditory relay?
A

Sections: Dorsal, medial, ventral

Main auditory relay: Ventral

147
Q
  1. What is the limit of phase locking in the MGB?
A

250 Hz (10% of neurons can reach 1000 Hz)

148
Q
  1. Outputs from MGB go where?
A

cortex

149
Q
  1. What are the 3 main areas of the auditory cortex?
A
  1. the core (A1)
  2. the belt (A2)
  3. the parabelt (Ep)
150
Q
  1. How many layers does the auditory cortex have? Is this the same or different as other cortical sensory processing centers?
A 
6 layers:
I: cell poor
II: small pyramidal cells
III: large pyramidal cells, fusiform
IV: stellates, pyramidal
V: 2 parts, cell sparse and dense
VI: pyramidal, complex arrangement.

This is the same as other cortical sensory processing centers

151
Q
  1. vMGB projects mainly to what layer of the auditory cortex?
A

the core (A1)

152
Q
  1. Explain the neural connections in layer IV.
A

cells organized in vertical columns and and have direct soma to soma connections—- no axons needed to conduct electricity. as long as one soma fires, the others will.

153
Q
  1. Explain the tonotopic organization of A1 (core) and A2 (belt).
A

A1: from low to high in the general area and on a single cell level (as shown by the location of low to high CF across the cortex (in mm). multiple arrangements of L->H and H–> L A1.
A2: no tonotopic organization; cells in same regions and can have various CFs

*tonotopicity gets complicated at the level of the cortex vs. at the cochlear and the AN

154
Q
  1. What are two things that make measuring response properties and classification very difficult in A1.
A

some areas tonotopically organized in iso-frequency strips (A1 sheet alignment vary across species).
some are organized into discrete columns.
physical state?????????

multiple tonopically arangemnets; b/c cells are so diff and get diff inputs, their response are too diverse

155
Q
  1. Design a neuron with convergent inputs that has improved tuning.
A

see IC lecture.

156
Q
  1. What are the two main divisions of the efferent system? Which one do we know more about?
A

caudal (more understood) and rostral systems.

understand below IC better than above

157
Q
  1. What are the 3 main feedback loops in the rostral portion? Which is the main auditory processing loop?
A

1st loop: AC/IC/vMGB- tonotopically organized
2nd loop: AC/IC/PTG- posterior thalamic group
3rd loop: AC/SC/MGB

1st loop?

158
Q
  1. The neurons in the LOCB originate from where? Do they mostly have crossed or uncrossed projections?
A

originate from LSO and surrounding area.

mostly uncrossed projections

159
Q
  1. The neurons in the MOCB originate from where? Do they mostly have crossed or uncrossed projections?
A

from MNTB,VNTB, DMPO, VMPO

mostly crossed, but still follow the LOCB fibers.

160
Q
  1. Describe the connections of MOCB fibers to IHCs and OHCs.
A

IHC: indirectly
OHC: directly

161
Q
  1. How do rate-intensity functions change with background noise? Noise + MOCB?
A

w/ Noise: greater firing rate at low level, but nerve reaches the hight of the firing rate as the tone alone at higher levels.
w/ Noise+ MOCB: less firing from the noise and better/larger DR (closer to the tone alone firing rate at high levels).

162
Q
  1. What is the average change in threshold for an ANF with MOCB stimulation?
A

15 dB

163
Q
  1. How does the cochlear microphonic change with MOCB stimulation?
A

CM increases by a few dB (at low and mid freq.)

164
Q
  1. How does the compound action potential change with MOCB stimulation?
A

suppressed

165
Q
  1. How does the summating potential change with MOCB stimulation?
A

suppressed

166
Q
  1. How does the endocochlear potential change with MOCB stimulation?
A

reduced by 6-7%

167
Q
  1. How does MOCB stimulation change hair cell polarization?
A

causes hyperpolarization

168
Q
  1. What is the end organ of sensation for the vestibular system?
A

cristae

169
Q
  1. How many semicircular canals are there?
A

3; superior, horizontal, and inferior semicircular canals

170
Q
  1. Which areas are able to determine linear motion? Angular motion?
A

linear (walking, falling, car travel): fluid within utricle and saccule
angular (rotation- head turns) : fluid within the 3SSC

171
Q
  1. What is the typical spontaneous rate of vestibular hair cells?
A

+90 spikes/sec

172
Q
  1. What is the cupula? What does it do?
A

gelatinous, dome shaped structure that fits within the walls of the labyrinth creating a fluid tight partition.
gravity matches the endolymph’s gravity

when endolymph is displaced pushes the partition in the opposite direction of the head turn
w/ displacement of the cupula–> shearing of the hair cells

173
Q
  1. If a head rotates and accelerates to the left, how do the left and right vestibular afferent fibers respond?
A

The left fibers are excitatory and the right are inhibitory.

HESP 653: Anatomy and Physiology (1 decks)

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