Physiology of Auditory and Vestibular Systems Flashcards
detects sounds and uses acoustic cues to identify and locate sound sources in the environment
auditory system
oscillations of air pressure that vary rapidly w/ time
sound
sound pressure (intensity) specified by a scale of sound pressure level in decibels (dB)
amplitude
number of oscillations of air pressure per second (Hz)
frequency
How does displacement of hair cells along the basilar membrane contribute to differences in sound frequency?
- the motion is a traveling wave from base of cochlea to apex where the wave patterns differ for different frequencies
- the basilar membrane varies in structure over its length
- the membrane near the base and oval/round windows is narrow/stiff and experiences maximal motion for high frequencies
- the membrane near the apex and helicotrema is wider/more flexible and experiences maximal motion for lower frequencies
sounds that cause greater deflection of the basilar membrane near the base where it is narrow/stiff
high frequency sounds
sounds that cause greater deflection of the basilar membrane near the helicotrema where it is loose/flexible
lower frequency sounds
- frequency of sound
- coded by where along the basilar membrane there is the greatest deflection
pitch
- polarized epithelial cells w/ basal and apical ends
- contain stereocilia on apical surface and neural synapses on basal side
- stiff, graded in size, and rich in actin
- cell type that receives afferent and efferent input, however they are not neuronal
- these cells are mechanoreceptors: convert mechanical signals to electrical signals
-
hair cells
- potassium-RICH fluid filling cochlear duct and membranous labyrinth
- bathes apical end of hair cells
- similar to ICF: high in K+, low in Na+
- found in scala media
- produced by stria vascularis
endolymph
- potassium-POOR fluid that bathes basal end of cochlear hair cells
- similar to ECF: high Na+, low K+
- found in scala vestibuli and scala tympani
perilymph
What are the differences between endolymph and perilymph at what do these differences contribute to?
- endolymph is high in K+ and found in scala media
- perilymph is low in K+ and found in scala vestibuli and scala tympani
- these differences in ion conc and location of fluid leads to a charge differential that readily allows K+ to flow into hair cells once the stereocilia have been deflected
How is an action potential generated by a hair cell?
- following deflection of stereocilia toward longest stereocilia, K+ ions enter cell and depolarize it
- stereocilia are connected to each other via tip links that transmit force to elastic gating spring (protein bridge), allowing the stereocilia to bend together and, in turn, open the cation gates (even small vibrations of 0.3 nm can cause channel opening)
- depolarization occurs when mechanically gated K+ cation channels open at apex of stereocilia and allow influx of K+
- depolarization causes the voltage-gated channels (TRPA1) to open, allowing Ca2+ to flow into the cell
- Ca2+ influx allows for further depolarization, causing the hair cell to release NT glutamate (excitatory) which generates an action potential in CN VIII
(at rest, hair cell is partially depolarized, however this is not enough to trigger an AP)
What does the directional deflection of stereocilia lead to?
(stereocilia linked together, thus they deflect as a bundle)
- deflection toward tallest stereocilia: depolarization
- deflection in opposite direction: hyperpolarization
How does the stria vascularis maintain electrochemical properties of the endolymph and contribute to sound conduction?
- located in lateral wall of cochlear duct (scala media) and produces endolymph w/ high K+ conc
- this creates high endocochlear potential (+80 mV) that drives positively charged ions into hair cell down their concentration gradient, thereby contributing to generation of AP
- this also forms the blood-labyrinth barrier (BLB)
What is the relationship between blood-labyrinth barrier, stria vascularis, and hearing loss?
- stria vascularis (SV) establishes the blood-labyrinth barrier (BLB) by prod endolymph which creates high endocochlear potential
- BLB is main site of drug entry to access inner hair cell, sometimes to its detriment
- any substance (meds, drugs, CO, etc) that disrupt SV function or damages SV will diminish endocochlear potential and impact hearing
- stria vascularis is a common source of ototoxic drug secretion into cochlea (crosses BLB)
What is the role of the inner and outer hair cells? How are they arranged?
- outer: acts as an amplifier, arranged in 3
- inner: primary source of auditory info, arranged in single row
Inner hair cells
- primary function:
- arrangement:
- synapses:
- efferent activity:
Inner hair cells
- primary function: primary source of auditory info
- arrangement: single layer
- synapses: synapse w/ the peripheral terminal of a primary afferent sensory neuron
- efferent activity: efferent neuron also modulates activity as well
Outer hair cells
- primary function:
- arrangement:
- synapses:
- efferent activity:
Outer hair cells
- primary function: amplify sound waves; contractile (boosts mechanical vibrations of basilar membrane, making them an amplifier)
- arrangement: 3 rows
- synapses: form a synapse w/ sensory afferent peripheral terminals from spiral ganglion
- efferent activity: form synapse w/ terminals from efferent neurons
What does the outer hair cell contractility lead to in terms of sound production?
- outer hair cell motility causes basilar membrane to move (retrograde) toward oval window and through middle ear via ossicles to cause displacement of tympanic membrane
- thus, ear itself can produce a sound (usually below our threshold to hear it)
- these impulses, olivocochlear efferents, arise in the SOC (medial portion innervates outer hair cells, lateral inner hair cells)
- sounds produced by outer hair cells’ retrograde movement
- can be measured in the external acoustic meatus (routinely done in infants as a hearing test)
- these sounds are usually inaudible (low intensity)
- two types: spontaneous (occurs in 1/3 of ppl, usually pure tones/clicks) and evoked (used for testing hearing loss, no emissions if damage present)
- clinical importance: newborn hearing screen, tinnitus (less evoked emissions due to conflicting sound waves), and ototoxicity
otoacoustic emissions
What is the general structural pathway of the auditory pathway?
cochlear nuclei
>
superior olivary complex
>
inferior colliculus
>
medial geniculate nucleus
>
auditory cortices
- branch point of the central portion of cochlear N.
- area that begins processing temporal and spectral features of sound
- nature of sound (high, low)
anterior cochlear nuclei
- branch point of the central portion of the cochlear nerve
- integrates acoustic info w/ somatosensory info
posterior cochlear nuclei
- first site in brainstem where info from both ears coverges
- binaural processing is essential to accurately localize sound
- contains medial part that generates a map of interaural time differences (localize location), and a lateral part that generates a map of interaural intensity differences (localize source)
superior olivary complex
- generates a map of the interaural time differences of arrival to ears
- helps localize location of sound
- receives excitatory (glutamate and/or aspartate) input
medial superior olivary nucleus (MSO)
- generates a map of the interaural intensity differences of sound between ears
- helps localize source of the sound
lateral superior olivary nucleus (LSO)
- suppresses info related to echoes, which would interfere w/ localization and arrival at final estimation of localization of sound along horizon
- info about time and intensity differences converge into this area
- info covergence and echo suppression together help create precise origin of sound location along horizon
- also thought to be a major contributor to tinnitus
inferior colliculus
- area in the thalamus that is a relay station in auditory pathway
- lots of convergence from distinct spectral and temporal pathways, allowing for processing features of speech inflections
- precise info regarding intensity, frequency, and binaural properties of sound are integrated and relayed onward
medial geniculate nucleus (MGN)
- essential for conscious perception of sound
- higher order processing of sound (loudness, modulations in volume, rate of frequency modulation)
primary auditory cortex (A1)
- composed of multiple areas (Broca’s Wernicke’s, etc)
- less specifically organized in tonotopic arrangement than PAC, but more integrated
- thought to respond to more complex sounds (music), identifying (naming) sounds, and speech
- maintains frequency organization from cochlea (more rostral areas are activated by low freq, more caudal areas respond to higher freq)
auditory association cortex (secondary auditory cortex)
What are the 3 types of efferents to the auditory system?
- olivocochlear efferents
- middle ear muscle motorneurons
- autonomic innervation of the inner ear
- efferents that originate in SOC
- decrease basilar membrane motion
- reduce responses of inner hair cells and auditory nerve fibers
- reduce response to noise
- may protect hair cells from damage due to intense sounds
- 2 aspects to these efferent fibers: 1) hair cell movement causes OAE (emission testing), and 2) reduces response to noise (protective)
olivocochlear efferents
- efferent motor innervation to tensor tympani to malleus and tympanic membrane and stapedius to stapes
- attenuates sound during loud/intense noises
- bilateral response evoked to high sound levels
- acts at low frequency, may prevent masking (improving speech discrimination)
- may prevent damage in hair cells due to intense sound
- implicated in tinnitus
middle ear efferents
- efferent innervation to inner ear may arise from:
1) CN VIII
2) caroticotympanic nerve off superior cervical ganglion: innervates mucous glands of tympanum and blood vessels of ear drum and contents
3) acoustic nerve supplies blood vessel sympathetics, regulates vascular tone in blood supply to cochlea - comprised of sympathetic adrenergic fibers
autonomic efferents
- caused by damage to hair cells, nerve fibers, or both
- causes: noise damage, ototoxic drugs, age related, or etiology unknown
- outer hair cells more susceptible to injury than inner due to them being first barrier to loud noise (receives stimulus first)
- injury to outer hair cells causes decrease in sensitivity and broader tuning
- injury to inner hair cells cuts off auditory input to CNS
- base (high freq) end is more susceptible to damage than apical (low freq) end because cochlear protective mechanisms work better for low freq sounds
- some hearing may be restored w/ cochlear prosthesis
sensorineural hearing loss
- multiple electrode wire threaded through cochlea to stimulate surviving nerve fibers
- if cochlear N. is completely damaged or there is an issue w/ the central pathway then this won’t work
cochlear prosthesis
rotation in verticle plane forwards maximally activates:
anterior semicircular canal
rotation in the horizontal plane is best detected by:
horizontal semicircular canal
rotation in vertical plane backwards maximally activates:
posterior semicircular canal
detects linear acceleration forward and backward
utricle
detects linear acceleration up and down
saccule
