Cochlear implants (CIs) function by directly depolarizing spiral ganglion neurons (SGNs) with current applied through an intracochlear array. While with prolonged deafness, SGN soma are lost, progressive structural changes, including loss of internodal myelin, precede complete degeneration. Speech reception performance in implantees and intracochlear-stimulation-induced spiking responses in animal models vary dramatically with duration of deafness preceding activation, and the contribution of myelination changes to these dynamics remains unknown. This proposal presents simulations exploring how the activity of model SGN axon populations in response to applied stimuli varies with their myelination state. Preliminary work describing a procedure for constructing model populations of SGN axons in different states of degeneration and demyelination stimulated extracellularly is presented. The proposed Aim 1 leverages simple stimuli to probe the basic electrophysiological properties of such populations, such as their refractoriness, temporal integration, and frequency following. These results will be interpreted in the context of recordings from SGN central axons of intracochlearly-stimulated animals at variable durations of deafness. Incorporation of demyelination and degeneration into these fiber populations is anticipated to yield changes like those in long-term deafened animals.
Aim 2 explores how stimuli used in human psychophysical envelope and fine temporal structure detection experiments are encoded by populations with different myelination states and degrees of fiber loss. This will provide insight into how stimulus features on different temporal scales are impacted by such pathological changes. Finally, Aim 3 employs carefully selected phoneme-like stimuli, either in quiet or masked by noise, applied to two independently selectable populations, in a simulated binaural discrimination experiment. This experimental approach will provide insight into how SGN structural pathology may differentially alter speech reception in noise and quiet. Collectively, these studies will provide insight into how pathology alters neural properties and, consequently, degrades coding of critical acoustic features. Understanding the distinct impacts of pathological changes on different facets of acoustic signal coding may pave the way for innovations in signal processing design tailored to a patient?s biological or situational demands.
This project seeks to understand how pathological, structural changes observed in the auditory nerve fibers (ANFs) of long-term deafened humans and animal alter those fibers capacity to encoding auditory signals delivered via cochlear implants. Demyelination and fiber-threshold-dependent degeneration will be incorporated into a previously characterized, biophysical population simulation of ANFs receiving extracellular stimulation, and these modifications? impacts on encoding of stimuli representing different acoustic features will be explored.
