This research examines brain mechanisms for processing of temporal information relevant to speech. Comparison of responses to acoustical and electrical (cochlear-implant) stimulation will help to isolate """"""""ear"""""""" from """"""""brain"""""""" components of temporal processing and will provide a basic-science foundation for design of speech processors for clinical cochlear prostheses. Acute and chronic auditory-cortex experiments in guinea pigs will employ acoustical and electrical stimulation. Psychophysical experiments in guinea pigs and in human cochlear-implant users will test predictions from the cortical studies.
Specific Aim 1 will characterize the cortical transformation of codes for amplitude modulation. Neurons in cortical input layers phase lock to to modulated electrical pulse trains at frequencies to >60 Hz. Temporal information that is fed forward to other cortical layers must be re-coded in a form that does not require tonic phase locking. We will test the hypothesis that high-frequency modulation information is transformed from a tonic phase-locking code to a rate code or phasic temporal code within the cortical columns of area A1.
This aim also tests 2 clinically relevant hypotheses: (1) Sensitivity to modulation of electrical pulse trains is optimized by monopolar electrode configurations and by carrier pulse rates low enough to permit entrainment in the auditory nerve or lower brainstem;and (2) Inter-channel interference is minimized by a pulse rates that permit inter-channel temporal separation of at least 500 jis.
Specific Aim 2 will distinguish peripheral and central mechanisms of temporal acuity and will identify factors that influence forward masking. We will test the hypothesis that forward masking reflects mechanisms within the central auditory system that are substantially distinct from the mechanisms of amplitude-modulation sensitivity. Our pilot results lead us to the hypothesis that forward masking in electrical hearing is minimized by the use of pulse rates that exceed maximum rates for entrainment of brainstem auditory structures.
Specific Aim 3 will quantify plasticity in transmission of temporal information resulting from deafening and chronic stimulation. We will test the hypothesis that temporal acuity of central structures improves during the first 30 days of cochlear-implant stimulation.
The aims of this study have direct application to deaf patients who use cochlear implants, particularly through influencing design of speech processors.
Aim 1 will identify factors that maximize the number of prosthesis channels that transmit non-redundant temporal information.
Aim 2 will identify factors that can restore forward masking to levels typical of normal hearing.
Aim 3 will identify changes in the central auditory pathway that result from deafness and chronic electrical stimulation and, thus, will inform decisions regarding age of implantation and patterns of chronic stimulation.
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