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Paul Faure (56)

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Paul Faure

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- synaptic neuron  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 Week 8
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