Binaural Processing Deficits Due to Synaptopathy and Myelin Defects

Area of Science:

• Auditory Neuroscience
• Computational Auditory Neuroscience
• Speech Perception

Background:

• Hidden hearing loss (HHL) presents as reduced speech intelligibility and perception despite normal audiometric thresholds.
• Potential causes include noise exposure, aging, and myelin defects, with peripheral auditory neuropathies implicated in animal models.
• Sound localization is crucial for speech comprehension, particularly in noise, and its impairment may contribute to HHL.

Purpose of the Study:

• To investigate the hypothesis that cochlear spiral ganglion neuron (SGN) neuropathies disrupt medial superior olive (MSO) activity, leading to sound localization deficits.
• To model the impact of SGN myelin defects (myelinopathy) and synapse loss (synaptopathy) on auditory processing.

Main Methods:

• Developed a computational network model of the auditory system, simulating peripheral responses and neural signal propagation.
• Incorporated biophysical SGN models with simulated myelinopathy and synaptopathy to mimic peripheral auditory neuropathies.
• Analyzed the impact of these simulated neuropathies on the interaural time difference (ITD) sensitivity of MSO neurons.

Main Results:

• Model simulations demonstrated that both SGN myelinopathy and synaptopathy significantly decrease the ITD sensitivity of MSO cells.
• This reduced ITD sensitivity suggests a potential neural mechanism underlying the sound localization deficits observed in HHL.

Conclusions:

• Cochlear spiral ganglion neuron neuropathies, specifically myelinopathy and synaptopathy, can disrupt auditory brainstem processing crucial for sound localization.
• The developed model provides insights into the downstream effects of SGN dysfunction on auditory perception and may aid in developing treatments for HHL.