This outline summarizes major points covered in lecture. It is not intended to replace your own lecture notes.
Haircell Receptor Potential (Intracellular)
In response to an acoustic stimulus, the IHCs electrical response has both a DC component (change in
baseline of receptor potential) and an AC component (corresponding to structure of stimulus frequency)
Amplitude of DC component grows with stimulus frequency; it dominates in IHCs.
Amplitude of AC component shrinks with stimulus frequency
AC component more important at low frequencies; it dominates in OHCs
The Action Potential Occurs in Nerve Fibers
As haircell becomes more depolarized, neurotransmitter is released to neuron connected to haircell
Neurotransmitter released from haircell receptor is received by specific membrane receptors on post-
Binding of neurotransmitter by the neural receptor causes ion channels to open in neural plasmalemma
which in turn causes the neuron’s membrane potential to become depolarized
Eventually, the neuron’s membrane potential reaches the threshold for an all-or-none action potential
Encoding Auditory Signals by IHC
Deformation of haircell stereocilia causes ion (potassium, K ) channels to open on IHC stereocilia.
Flow of potassium causes de+2larization of haircell receptor (graded potential), and the opening of
voltage-gated calcium (Ca ) channels
Increase in intracellular [Ca ] leads to further depolarization and release of glutamate neurotransmitter
from IHC receptor, and also the active exiting mechanism for K +
Binding of glutamate by receptors on cell membrane of Type I radial afferents leads to depolarization and
generation of all-or-none action potential (spike) in sensory neuron.
Electrophysiologists study the number, timing and pattern of spike discharges to acoustic stimulus
Outer Haircells (OHCs)
Function of OHCs: believed to modify incoming information and provide auditory system with high
sensitivity and resolution for stimulus frequency and amplitude
OHCs feedback energy to cochlea; thought to affect motility of tectorial membrane
OHCs can act as a cochlear amplifier – provide gain for the system.
Mechano- to neurotransduction mechanism probably similar as what is observed in IHC
Acoustic stimulus causes OHC to contract (i.e. OHC have motility).
Contraction of OHC will vary stereocilia contact with tectorial membrane
OHC size varies along cochlear length (and thus sound frequency that they respond to)
OHC Size Changes Along Cochlea
OHC length, not diameter, varies with position (and thus characteristic frequency)
During acoustic stimulation, OHCs contract (length decreases) and then expand (length increases)
Contraction cycles occur on cycle-by-cycle basis with stimulus
Contraction affects amplitude and frequency sensitivity (stereocilia attached to tectorial membrane)
Otoacoustic Emissions (OAE)
Ear produces weak sounds on its own (i.e. otoacoustic emissions)
OAEs are not echoes reflected in external auditory canal
The amplitude of evoked otoacoustic emissions (EOAEs) increases with stimulus SPL
Different types of OAEs
i. SEOAE – spontaneously evoked otoacoustic emissions
ii. TEOAE – transiently evoked otoacoustic emissions
iii. DPOAE – distortion product otoacoustic emissions (e.g. cubic difference tone: 2f – 1 ) 2
DPOAE is evidence for non-linearity of auditory system
Psych 3A03 18 October 2012