Biology subjects

Tollin, D. J.

Publications and source records attributed to Tollin, D. J..

5 recordsLinked to original sources

bioRxiv2026

Persistent impairment of spatial hearing and neural binaural interaction after temporary noise-induced hearing loss

Many people have trouble understanding speech in noisy environments despite normal audiometric thresholds, a condition referred to as "hidden hearing loss." A leading hypothesis attributes this deficit to inner hair cell synaptic pathology (cochlear synaptopathy), which can persist after recovery from noise-induced temporary elevation of audiometric thresholds. This pathology impairs the temporally precise sound encoding necessary for spatial hearing, but direct evidence in primates, human or nonhuman, is lacking. Here, we show that a single noise exposure, producing only a temporary threshold elevation, induced long-lasting alterations in synaptic morphology, without synapse loss, resulting in persistent spatial hearing deficits for up to 11 months post-exposure in nonhuman primates of both sexes. These perceptual deficits were accompanied by a reduction in a neurophysiological measure of binaural processing - the binaural interaction component (BIC) of the auditory brainstem response (ABR). Both behavioral and neural deficits persisted despite full recovery of audiometric thresholds. Together, these findings provide the first evidence in primates that noise exposure disrupts spatial hearing and binaural neural circuit function without loss of hair cells or synapses. Because spatial hearing tests and the ABR/BIC are clinically accessible, this work also establishes translational biomarkers for early neural dysfunction underlying hidden hearing loss.

neuroscience↗

bioRxiv2025

Speech Processing Development in Infants: A Longitudinal ERP Study of Native and Nonnative Consonant Discrimination

BackgroundPerceptual attunement theory predicts that during the first year of life, infants neural responses to native speech sounds should strengthen while responses to nonnative contrasts diminish. However, few longitudinal studies have directly tested these predictions using within-subject designs. MethodsWe recorded auditory event-related potentials (ERPs) from 84 typically developing infants at three time points (3, 6, and 12 months) using an oddball paradigm with native (/ba/-/da/) and nonnative (dental vs. retroflex /a/) consonant contrasts. We examined developmental trajectories of the mismatch response (MMR) and obligatory components (P1, N1, P2) using linear mixed-effects models, with Session x Language interactions testing differential development for native versus nonnative contrasts. Center of mass analysis characterized spatial reorganization of ERP topography across development. ResultsContrary to perceptual attunement predictions, most ERP measures showed similar developmental trajectories for native and nonnative consonants. Of 14 interaction tests, only N1 latency for deviant waveforms showed a significant Session x Language interaction (p = 0.046, p{superscript 2} = 0.025). Significant main effects of Session on multiple measures confirmed ongoing auditory maturation. Center of mass analysis revealed systematic spatial reorganization: P1 showed posterior migration and leftward shifts (0.078 units displacement), while N1 and MMR exhibited anterior shifts, with nonnative consonants showing larger spatial reorganization for N1 (0.099 units vs. 0.058 units for native). ConclusionsRobust neural signatures of perceptual attunement for consonants may be more subtle, later-emerging, or stimulus-specific than commonly assumed. The dissociation between stable amplitude and migrating generators suggests that spatial location may be as important as response magnitude for characterizing auditory maturation during early infancy. Practically, equivalent neural responses to native and nonnative consonant contrasts should not be interpreted as evidence of atypical development; rather, indices of general auditory maturation may be more reliable markers of healthy development during the first year.

physiology↗

bioRxiv2024

Unilateral auditory deprivation reveals brainstem origin of a sensitive period for spatial hearing

Early sensory experience can exert lasting perceptual consequences. For example, a brief period of auditory deprivation early in life can lead to persistent spatial hearing deficits. Some forms of hearing loss (i.e., conductive; CHL) can distort acoustical cues needed for spatial hearing, which depend on inputs from both ears. We hypothesize that asymmetric acoustic input during development disrupts auditory circuits that integrate binaural information. Here, we identify prolonged maturation of the binaural auditory brainstem in the guinea pig by tracking auditory evoked potentials across development. Using this age range, we induce a reversible unilateral CHL and ask whether behavioral and neural maturation are disrupted. We find that developmental CHL alters a brainstem readout of binaural function which is not observed when the CHL is induced in adulthood. Startle-based behavioral measures reveal poorer spatial resolution of sound sources, but only for high-frequency sound stimuli. Finally, single-unit recordings of auditory midbrain neurons reveal significantly poorer neural acuity to a sound location cue that largely depends on high-frequency sounds. Thus, these findings show that unilateral deprivation can disrupt developing auditory circuits that integrate binaural information and may give rise to lingering spatial hearing deficits.

neuroscience↗

bioRxiv2023

The rapid decline in interaural-time-difference sensitivity for pure tones is explained by a single frequency-channel model

PurposeThe interaural time difference (ITD) is a primary horizontal-plane sound localization cue computed in the auditory brainstem. ITDs are accessible in the temporal fine structure of pure tones with a frequency of no higher than about 1400 Hz. Explaining how listeners ITD sensitivity transitions from very best sensitivity near 700 Hz to impossible to detect within 1 octave currently lacks a fully compelling physiological explanation. Here, it was hypothesized that the rapid decline in ITD sensitivity is dictated not by a central neural limitation but by initial peripheral sound encoding, specifically, the low-frequency (apical) edge of the cochlear excitation pattern produced by a pure tone. MethodsITD sensitivity was measured in 16 normal-hearing listeners as a joint function of frequency (900-1500 Hz) and level (10-50 dB sensation level). ResultsPerformance decreased with increasing frequency and decreasing sound level. The slope of performance decline was 90 dB/octave, consistent with the low-frequency slope of the cochlear excitation pattern. ConclusionFine-structure ITD sensitivity near 1400 Hz may be conveyed primarily by "off-frequency" activation of neurons tuned to lower frequencies near 700 Hz. Physiologically, this could be realized by having neurons sensitive to fine-structure ITD up to only about 700 Hz. A more extreme model would have only a single narrow channel near 700 Hz that conveys fine-structure ITDs. Such a model is a major simplification and departure from the classic formulation of the binaural display, which consists of a matrix of neurons tuned to a wide range of relevant frequencies and ITDs.

neuroscience↗

bioRxiv2019

Auditory binaural and spatial hearing impairments in a Fragile X Syndrome mouse model

The auditory brainstem compares sound-evoked excitation and inhibition from both ears to compute sound source location. Although alterations to the anatomy and physiology of the auditory brainstem have been demonstrated in Fragile X Syndrome (FXS) it is not known whether these changes cause sound localization impairments in FXS. To test the hypothesis that FXS-related alterations to brainstem circuits impair spatial hearing abilities, a reflexive prepulse inhibition (PPI) task, with sound source location as the prepulse stimulus, was used to show that Fmr1 knockout mice have decreased inhibition of their startle responses. Specifically, Fmr1 mice show decreased PPI compared to wildtype during gap detection, changes in sound source location, and spatial release from masking with no alteration to their overall startle thresholds compared to wildtype. Lastly, Fmr1 mice have increased latency to respond in these tasks suggesting additional impairments in the pathway responsible for reacting to a startling sound.

neuroscience↗