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Modifying the Auditory Nerve InputModifying the Auditory Nerve Input
to a Computational Model of theto a Computational Model of the
Dorsal Cochlear NucleusDorsal Cochlear Nucleus
Adam GiangAdam Giang
Spring 2008Spring 2008
Boston University College of Engineering
OverviewOverview
ObjectiveObjective
Auditory System and ModelingAuditory System and Modeling
Techniques (Background Information)Techniques (Background Information)
Experimental ProcedureExperimental Procedure
ResultsResults
SummarySummary
ObjectiveObjective
Study the effects of auditory trauma on theStudy the effects of auditory trauma on the
brain’s interpretation of soundbrain’s interpretation of sound
Simulate impaired auditory nerve (AN) andSimulate impaired auditory nerve (AN) and
dorsal cochlear nucleus (DCN) usingdorsal cochlear nucleus (DCN) using
computational modelscomputational models
Evaluate models’ effectiveness in aEvaluate models’ effectiveness in a
physiological contextphysiological context
Modeling the Auditory SystemModeling the Auditory System
Sound
Pressure
Signal s(t)
AN
Model
DCN
Model
Response
Maps
BruceBruce AuditoryAuditory NerveNerve
ModelModel
Project uses Auditory Nerve model as described by ZilanyProject uses Auditory Nerve model as described by Zilany
and Bruce (2006)and Bruce (2006)
Input: Instantaneous Pressure WaveformInput: Instantaneous Pressure Waveform
Output: Spike Train (Action Potentials)Output: Spike Train (Action Potentials)
Allows for inner (IHC) and outer (OHC) cochlear hair cellAllows for inner (IHC) and outer (OHC) cochlear hair cell
impairmentimpairment
DCN ModelDCN Model
DCN model asDCN model as
described by Hancockdescribed by Hancock
and Voigt (1999)and Voigt (1999)
5 cell groups of 8005 cell groups of 800
isofrequency slicesisofrequency slices
spaced 0.005 octavesspaced 0.005 octaves
apart and centered atapart and centered at
5 kHz5 kHz
P cell behaviorP cell behavior
dependent ondependent on
connection parametersconnection parameters
NeuronNeuron ModelModel
Neuron model based on MacGregor neuromime (1987)Neuron model based on MacGregor neuromime (1987)
Each neuron modeled as a parallel circuit withEach neuron modeled as a parallel circuit with
membrane capacitance, leakage conductance, amembrane capacitance, leakage conductance, a
potassium channel branch, and excitatory/inhibitorypotassium channel branch, and excitatory/inhibitory
connection branchesconnection branches
MethodsMethods
AN Model Input: Wide Range of tonal stimulusAN Model Input: Wide Range of tonal stimulus
with intensity varying from 0 to 90 dB SPL in 6with intensity varying from 0 to 90 dB SPL in 6
dB SPL increments and frequency varying in 1.5dB SPL increments and frequency varying in 1.5
Octave band above and below 5 kHzOctave band above and below 5 kHz
Spike Trains Generated by AN model inputtedSpike Trains Generated by AN model inputted
into DCN modelinto DCN model
Response Maps generated for a wide range ofResponse Maps generated for a wide range of
connection Parametersconnection Parameters
Sound
Pressure
Signal s(t)
AN
Model
DCN
Model
Response
Maps
RateRate Level CurvesLevel Curves
TuningTuning CurvesCurves
ResponseResponse Maps IMaps I
Increasing OHC impairment
Blue: Excitatory Response
Red: Inhibitory Response
Gray: Spontaneous Activity
Response Maps IIResponse Maps II
Increasing IHC impairment
Blue: Excitatory Response
Red: Inhibitory Response
Gray: Spontaneous Activity
Response Maps IIIResponse Maps III
Total hair cell impairmentHealthy AN fiber
ConclusionsConclusions
Impaired AN models exhibit elevated thresholds,Impaired AN models exhibit elevated thresholds,
broadened tuning, and shifted rate-level curves,broadened tuning, and shifted rate-level curves,
consistent with physiological dataconsistent with physiological data
DCN response maps show a decrease inDCN response maps show a decrease in
regions of both excitation and inhibition, coupledregions of both excitation and inhibition, coupled
with an increase in spontaneous areas (tinnitus)with an increase in spontaneous areas (tinnitus)
Connection parameters for DCN model whichConnection parameters for DCN model which
best modelbest model physiological responses still to bephysiological responses still to be
determineddetermined
Future use of models to reveal insight intoFuture use of models to reveal insight into
hearing loss and auditory system itselfhearing loss and auditory system itself
Healthy Response Map MatrixHealthy Response Map Matrix
Fully Impaired OHCFully Impaired OHC

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Modifying Auditory Nerve Input to DCN Model

  • 1. Modifying the Auditory Nerve InputModifying the Auditory Nerve Input to a Computational Model of theto a Computational Model of the Dorsal Cochlear NucleusDorsal Cochlear Nucleus Adam GiangAdam Giang Spring 2008Spring 2008 Boston University College of Engineering
  • 2. OverviewOverview ObjectiveObjective Auditory System and ModelingAuditory System and Modeling Techniques (Background Information)Techniques (Background Information) Experimental ProcedureExperimental Procedure ResultsResults SummarySummary
  • 3. ObjectiveObjective Study the effects of auditory trauma on theStudy the effects of auditory trauma on the brain’s interpretation of soundbrain’s interpretation of sound Simulate impaired auditory nerve (AN) andSimulate impaired auditory nerve (AN) and dorsal cochlear nucleus (DCN) usingdorsal cochlear nucleus (DCN) using computational modelscomputational models Evaluate models’ effectiveness in aEvaluate models’ effectiveness in a physiological contextphysiological context
  • 4. Modeling the Auditory SystemModeling the Auditory System Sound Pressure Signal s(t) AN Model DCN Model Response Maps
  • 5. BruceBruce AuditoryAuditory NerveNerve ModelModel Project uses Auditory Nerve model as described by ZilanyProject uses Auditory Nerve model as described by Zilany and Bruce (2006)and Bruce (2006) Input: Instantaneous Pressure WaveformInput: Instantaneous Pressure Waveform Output: Spike Train (Action Potentials)Output: Spike Train (Action Potentials) Allows for inner (IHC) and outer (OHC) cochlear hair cellAllows for inner (IHC) and outer (OHC) cochlear hair cell impairmentimpairment
  • 6. DCN ModelDCN Model DCN model asDCN model as described by Hancockdescribed by Hancock and Voigt (1999)and Voigt (1999) 5 cell groups of 8005 cell groups of 800 isofrequency slicesisofrequency slices spaced 0.005 octavesspaced 0.005 octaves apart and centered atapart and centered at 5 kHz5 kHz P cell behaviorP cell behavior dependent ondependent on connection parametersconnection parameters
  • 7. NeuronNeuron ModelModel Neuron model based on MacGregor neuromime (1987)Neuron model based on MacGregor neuromime (1987) Each neuron modeled as a parallel circuit withEach neuron modeled as a parallel circuit with membrane capacitance, leakage conductance, amembrane capacitance, leakage conductance, a potassium channel branch, and excitatory/inhibitorypotassium channel branch, and excitatory/inhibitory connection branchesconnection branches
  • 8. MethodsMethods AN Model Input: Wide Range of tonal stimulusAN Model Input: Wide Range of tonal stimulus with intensity varying from 0 to 90 dB SPL in 6with intensity varying from 0 to 90 dB SPL in 6 dB SPL increments and frequency varying in 1.5dB SPL increments and frequency varying in 1.5 Octave band above and below 5 kHzOctave band above and below 5 kHz Spike Trains Generated by AN model inputtedSpike Trains Generated by AN model inputted into DCN modelinto DCN model Response Maps generated for a wide range ofResponse Maps generated for a wide range of connection Parametersconnection Parameters Sound Pressure Signal s(t) AN Model DCN Model Response Maps
  • 11. ResponseResponse Maps IMaps I Increasing OHC impairment Blue: Excitatory Response Red: Inhibitory Response Gray: Spontaneous Activity
  • 12. Response Maps IIResponse Maps II Increasing IHC impairment Blue: Excitatory Response Red: Inhibitory Response Gray: Spontaneous Activity
  • 13. Response Maps IIIResponse Maps III Total hair cell impairmentHealthy AN fiber
  • 14. ConclusionsConclusions Impaired AN models exhibit elevated thresholds,Impaired AN models exhibit elevated thresholds, broadened tuning, and shifted rate-level curves,broadened tuning, and shifted rate-level curves, consistent with physiological dataconsistent with physiological data DCN response maps show a decrease inDCN response maps show a decrease in regions of both excitation and inhibition, coupledregions of both excitation and inhibition, coupled with an increase in spontaneous areas (tinnitus)with an increase in spontaneous areas (tinnitus) Connection parameters for DCN model whichConnection parameters for DCN model which best modelbest model physiological responses still to bephysiological responses still to be determineddetermined Future use of models to reveal insight intoFuture use of models to reveal insight into hearing loss and auditory system itselfhearing loss and auditory system itself
  • 15. Healthy Response Map MatrixHealthy Response Map Matrix
  • 16. Fully Impaired OHCFully Impaired OHC

Editor's Notes

  1. Clean this up
  2. clean
  3. Sound travels through ear canal to cochlea, IHC and OHC connect via AN to DCN, located on brain stem and is site of complex auditory processing. OHC pre-amplifier and IHC transducer, converting sound pressure signal to electrical signal. The way we model this system is…
  4. 3 filters, c1 low level, c2 high level, control path filter regulates gain and bandwidth, note impairment parameters
  5. Rate level curves plot average firing rate versus sound level, increase with sound level until saturation. Shift in curves for ohc, ihc more dramatic shift, which dominates when both are impaired.
  6. Tuning curves plot threshold dB versus frequency (in this case, sound pressure level that causes firing rate of 30/s). Impairing OHC causes elevated thresholds and broadened tuning. Impairing IHC had similar effects but without broadened tuning.
  7. Response maps plot excitatory and inhibitory respones to stimulus on a sound pressure level vs. frequency plane. Impairing OHC caused a drop in low level responses. We also observed a favoring of excitatory over inhibitory response, agreeing with the physiological observations of Ma and Young
  8. Impairing IHC had similar results of decreased low level responses and a favoring of excitation over inhibition. Impairing IHC also caused a drop in mid level responses
  9. Impairing all hair cells leads to mainly spontaneous activity, and the chart looks like IHC impairment alone (since its effect encompasses that of the OHC).