Auditory Research publications

Objectives: This study aimed to evaluate the informational component of speech-on-speech masking. Speech perception in the presence of a competing talker involves not only informational masking (IM) but also a number of masking processes involving interaction of masker and target energy in the auditory periphery. Such peripherally generated masking can be eliminated by presenting the target and masker in opposite ears (dichotically). However, this also reduces IM by providing listeners with lateralization cues that support spatial release from masking (SRM). In tonal sequences, IM can be isolated by rapidly switching the lateralization of dichotic target and masker streams across the ears, presumably producing ambiguous spatial percepts that interfere with SRM. However, it is not clear whether this technique works with speech materials. Design: Speech reception thresholds (SRTs) were measured in 17 young normal-hearing adults for sentences produced by a female talker in the presence of a competing male talker under three different conditions: diotic (target and masker in both ears), dichotic, and dichotic but switching the target and masker streams across the ears. Because switching rate and signal coherence were expected to influence the amount of IM observed, these two factors varied across conditions. When switches occurred, they were either at word boundaries or periodically (every 116 msec) and either with or without a brief gap (84 msec) at every switch point. In addition, SRTs were measured in a quiet condition to rule out audibility as a limiting factor. Results: SRTs were poorer for the four switching dichotic conditions than for the nonswitching dichotic condition, but better than for the diotic condition. Periodic switches without gaps resulted in the worst SRTs compared to the other switch conditions, thus maximizing IM. Conclusions: These findings suggest that periodically switching the target and masker streams across the ears (without gaps) was the most efficient in disrupting SRM. Thus, this approach can be used in experiments that seek a relatively pure measure of IM, and could be readily extended to translational research.

Partial hearing loss can cause neurons in the auditory and audiovisual cortices to increase their responsiveness to visual stimuli; however, behavioral studies in hearing-impaired humans and rats have found that the perceptual ability to accurately judge the relative timing of auditory and visual stimuli is largely unaffected. To investigate the neurophysiological basis of how audiovisual temporal acuity may be preserved in the presence of hearing loss-induced crossmodal plasticity, we exposed adult rats to loud noise and two weeks later performed in vivo electrophysiological recordings in two neighboring regions within the lateral extrastriate visual (V2L) cortex—a multisensory zone known to be responsive to audiovisual stimuli (V2L-Mz) and a predominantly auditory zone (V2L-Az). To examine the cortical layer-specific effects at the level of postsynaptic potentials, a current source density (CSD) analysis was applied to the local field potential (LFP) data recorded in response to auditory and visual stimuli presented at various stimulus onset asynchronies (SOAs). As predicted, differential effects were observed in the neighboring cortical regions’ postnoise exposure. Most notably, an analysis of the strength of multisensory response interactions revealed that V2L-Mz lost its sensitivity to the relative timing of the auditory and visual stimuli, due to an increased responsiveness to visual stimulation that produced a prominent audiovisual response irrespective of the SOA. In contrast, not only did the V2L-Az in noise-exposed rats become more responsive to visual stimuli but neurons in this region also inherited the capacity to process audiovisual stimuli with the temporal precision and specificity that was previously restricted to the V2L-Mz. Thus, the present study provides the first demonstration that audiovisual temporal processing can be preserved following moderate hearing loss via compensatory plasticity in the higher-order sensory cortices that is ultimately characterized by a functional transition in the cortical region capable of temporal sensitivity.

Objective. The effects of lead exposure on cognitive function have been studied intensively over the past decade, but less attention has focused on its impact on auditory function. This study is aimed at investigating the effect of lead on the cochlea and the molecular mechanisms responsible for its actions. Methods. 0.2% lead acetate was administered to rats in drinking water for 30, 60, and 90 days. Brainstem auditory evoked responses (ABR) were recorded, and morphological changes in the hair cells were observed. We also measured glutathione (GSH) and malondialdehyde (MDA) concentrations and antioxidant enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) activities in the cochlea. Results. Lead exposure increased the ABR threshold and slightly prolonged the latencies of wave II and wave IV in rats. Abnormally shaped hair cells and loss of hair cells were found in the cochlea basilar membrane, together with degenerative changes in spiral ganglion neurons following lead exposure. The activities of some antioxidant enzymes were also reduced in association with upregulation of MDA expression. These effects may be caused by impaired catalytic function of the enzymes as a result of lead interaction. Conclusion. The antioxidant system of the cochlea in the immature rat brain is highly vulnerable to developmental lead exposure. Oxidative stress may therefore represent a possible mechanism for lead-induced auditory deficits.

In this study, we investigated the role of MAP kinase phosphatase-1 (MKP-1) and rosiglitazone (RSG) in glucocorticoid resistance and glucocorticoid sensitivity, respectively, using a guinea pig model of lipopolysaccharide- (LPS-) induced sudden sensorineural hearing loss (SSHL). The pigs were divided into control, LPS, LPS+dexamethasone (DEX), LPS+RSG, and LPS+DEX+RSG groups. Their hearing was screened by auditory brainstem response measurement. Immunofluorescence staining was used to identify the location of MKP-1 in the inner ear. The expression levels of MKP-1 and the related proteins in the inner ear were detected using western blotting. The morphological changes in the cochlea were observed via hematoxylin-eosin staining. Severe hearing loss was observed in the LPS group, as opposed to the protection from hearing loss observed in the LPS+DEX+RSG group. A positive correlation was observed between MKP-1 expression levels and protection from hearing loss. RSG and DEX synergistically influenced inner ear inflammation. In conclusion, resistance of LPS-induced SSHL guinea pig models to glucocorticoids may result from impaired MKP-1 function in inner ear tissues, induced by glucocorticoids, impairing the inhibition of inflammation. Our findings present novel targets to develop potential therapeutics to treat inflammatory diseases of the inner ear.

Accurate sound localization requires normal binaural input and precise auditory neuronal representation of sound spatial locations. Previous studies showed that unilateral hearing loss profoundly impaired the sound localization abilities. However, the underlying neural mechanism is not fully understood. Here, we investigated how chronic unilateral conductive hearing loss (UCHL) affected the neural tuning to sound source azimuth in the primary auditory cortex (AI). The UCHL was manipulated by the removal of tympanic membrane and malleus in the right ear of young (P14) rats and adult (P57) rats. We recorded the azimuth tuning of neurons in the left AI contralateral to the operated ear in the two groups of rats that experienced 2 months of UCHL, and in the left AI of age-matched control rats. We found that AI neurons in control rats showed predominant preference to sound from contralateral azimuths. However, UCHL weakened the cortical neuronal representation of contralateral azimuths on the operated ear side and strengthened the cortical neuronal representation of ipsilateral azimuths on the intact ear side. This effect was stronger in rats with UCHL at young age than in rats with UCHL in adulthood. Moreover, UCHL degraded the azimuth selectivity and azimuth sensitivity of AI neurons, and this effect was stronger in rats with UCHL in adulthood than in rats with UCHL at young age. These findings highlight a remarkable age-related experience-dependent plasticity of neural tuning to sound source azimuth in AI, and imply a neural mechanism for the impacts of chronic UCHL on sound localization abilities.

Objective: The purpose of this study was to investigate perceptual and electrophysiological encoding of complex periodic signals as a function of age. Design: Two groups of adults completed three listening tasks: a behavioural task of detection of a mistuned harmonic component in a complex tone, an electrophysiological measure of speech-evoked auditory brainstem response (sABR), and a speech-in-noise measure. Between group comparisons were undertaken for each task as well as pairwise correlation analyses for all tasks. Study sample: One group of younger adults (n = 20) and one group of older adults (n = 20) participated. All listeners had relatively normal audiometric thresholds (≤20 dB HL) from 250-4000 Hz. Results: Younger adults had better results than the older adults on all three tasks: sensitivity for detecting a mistuned harmonic, spectral encoding for sABR, and release from masking for the speech-in-noise test. There were no significant correlations between measures when evaluating the older adults in isolation. Conclusions: The results are consistent with the body of literature that demonstrates reduced temporal processing abilities for older adults. The combined method approach undertaken in this investigation did not result in correlations between the perceptual and electrophysiological measures of temporal processing.

Inferior olivary activity causes both short-term and long-term changes in cerebellar output underlying motor performance and motor learning. Many of its neurons engage in coherent subthreshold oscillations and are extensively coupled via gap junctions. Studies in reduced preparations suggest that these properties promote rhythmic, synchronized output. However, the interaction of these properties with torrential synaptic inputs in awake behaving animals is not well understood. Here we combine electrophysiological recordings in awake mice with a realistic tissue-scale computational model of the inferior olive to study the relative impact of intrinsic and extrinsic mechanisms governing its activity. Our data and model suggest that if subthreshold oscillations are present in the awake state, the period of these oscillations will be transient and variable. Accordingly, by using different temporal patterns of sensory stimulation, we found that complex spike rhythmicity was readily evoked but limited to short intervals of no more than a few hundred milliseconds and that the periodicity of this rhythmic activity was not fixed but dynamically related to the synaptic input to the inferior olive as well as to motor output. In contrast, in the long-term, the average olivary spiking activity was not affected by the strength and duration of the sensory stimulation, while the level of gap junctional coupling determined the stiffness of the rhythmic activity in the olivary network during its dynamic response to sensory modulation. Thus, interactions between intrinsic properties and extrinsic inputs can explain the variations of spiking activity of olivary neurons, providing a temporal framework for the creation of both the short-term and long-term changes in cerebellar output.

Our system separates simultaneous voices and compares them with brain waves of a listener to amplify attended speech.

Cisplatin-induced early-onset ototoxicity is linked to hearing loss. The mechanism by which cisplatin causes ototoxicity remains unclear. The purpose of this study was to identify the involvement of receptor-interacting protein kinase (RIP)3-dependent necroptosis in cisplatin-induced ototoxicity in vitro and in vivo. Sprague–Dawley rats (SD, 8 week) were treated via intraperitoneal (i.p.) injection with cisplatin (16 mg/kg for 1 day), and their hearing thresholds were measured by the auditory brainstem response (ABR) method. Hematoxylin and eosin (H & E) staining, immunohistochemistry, and western blots were performed to determine the effect of cisplatin-induced ototoxicity on cochlear morphology. Inhibitor experiments with necrostatin 1 (Nec-1) and Z-VAD were also performed in HEI-OC1 cell line. H&E stains revealed that the necroptotic changes were increased in the organ of Corti (OC) and spiral ganglion neurons (SGNs). Moreover, immunohistochemistry and western blot analysis showed that cisplatin treatment increased the protein levels of RIP3 in both OCs and SGNs. The treatment of Nec-1, a selective RIP1 inhibitor, resulted in markedly suppression of cisplatin-induced cell death in HEI-OC1 cells, whereas Z-VAD treatment did not change the cisplatin-induced cell death. Our results suggest that RIP3-dependent necroptosis was substantial in cisplatin-induced ototoxicity; inner cochlear regions, the OCs, and SGNs were especially sensitive to necroptosis.

A noise-induced loss of inner hair cell (IHC) - auditory nerve synaptic connections has been suggested as a factor that can trigger the progression of maladaptive plastic changes leading to noise-induced tinnitus. The present study used a military relevant small arms fire (SAF)-like noise (50 biphasic impulses over 2.5 min at 152 dB SPL given unilaterally to the right ear) to induce loss (∼1/3) of IHC synaptic ribbons (associated with synapse loss) in rat cochleae with only minor (less than 10%) loss of outer hair cells. Approximately half of the noise-exposed rats showed poorer Gap Detection post-noise, a behavioral indication suggesting the presence of tinnitus. There was significantly greater loss of IHC ribbons in noise-exposed rats with reduced Gap Detection compared to noise-exposed rats retaining normal Gap Detection. We have previously shown systemic administration of piribedil, memantine, and/or ACEMg significantly reduced loss of IHC ribbons induced by a 3 h 4 kHz octave band 117 dB (SPL) noise. The present study examined if this treatment would also reduce ribbon loss from the SAF-like noise exposure and if this would prevent the reduced Gap Detection. As in the previous study, piribedil, memantine, and ACEMg treatment significantly reduced the noise-induced loss of ribbons, such that it was no longer significantly different from normal. However, it did not prevent development of the reduced Gap Detection indication of tinnitus in all treated noise-exposed rats, reducing the incidence but not reaching significance.

To evaluate the ability of a restricted range of auditory-nerve fibers to encode a large perceptual dynamic range, Viemeister [(1983). Science 221, 1206–1208] examined the detection of a change in the level of a high-frequency band of noise flanked by more intense fixed-level noise maskers. Here, stimuli and procedures similar to Viemeister's were used, but random manipulations of level and notch cutoff frequency were included to evaluate predictions of energy-based models. The results indicate that cues other than the change in level per se are available, and suggest the potential contribution of changes in pitch/timbre for this task.

In neural circuits, action potentials (spikes) are conventionally caused by excitatory inputs whereas inhibitory inputs reduce or modulate neuronal excitability. We previously showed that neurons in the superior paraolivary nucleus (SPN) require solely synaptic inhibition to generate their hallmark offset response, a burst of spikes at the end of a sound stimulus, via a post-inhibitory rebound mechanism. In addition SPN neurons receive excitatory inputs, but their functional significance is not yet known. Here we used mice of both sexes to demonstrate that in SPN neurons, the classical roles for excitation and inhibition are switched, with inhibitory inputs driving spike firing and excitatory inputs modulating this response. Hodgkin–Huxley modeling suggests that a slow, NMDA receptor (NMDAR)-mediated excitation would accelerate the offset response. We find corroborating evidence from in vitro and in vivo recordings that lack of excitation prolonged offset-response latencies and rendered them more variable to changing sound intensity levels. Our results reveal an unsuspected function for slow excitation in improving the timing of post-inhibitory rebound firing even when the firing itself does not depend on excitation. This shows the auditory system employs highly specialized mechanisms to encode timing-sensitive features of sound offsets which are crucial for sound-duration encoding and have profound biological importance for encoding the temporal structure of speech.

Objectives: The aims of this study were to systematically explore the effects of stimulus duration, background (quiet versus noise), and three consonant–vowels on speech-auditory brainstem responses (ABRs). Additionally, the minimum number of epochs required to record speech-ABRs with clearly identifiable waveform components was assessed. The purpose was to evaluate whether shorter duration stimuli could be reliably used to record speech-ABRs both in quiet and in background noise to the three consonant–vowels, as opposed to longer duration stimuli that are commonly used in the literature. Shorter duration stimuli and a smaller number of epochs would require shorter test sessions and thus encourage the transition of the speech-ABR from research to clinical practice. Design: Speech-ABRs in response to 40 msec [da], 50 msec [ba] [da] [ga], and 170 msec [ba] [da] [ga] stimuli were collected from 12 normal-hearing adults with confirmed normal click-ABRs. Monaural (right-ear) speech-ABRs were recorded to all stimuli in quiet and to 40 msec [da], 50 msec [ba] [da] [ga], and 170 msec [da] in a background of two-talker babble at +10 dB signal to noise ratio using a 2-channel electrode montage (Cz-Active, A1 and A2-reference, Fz-ground). Twelve thousand epochs (6000 per polarity) were collected for each stimulus and background from all participants. Latencies and amplitudes of speech-ABR peaks (V, A, D, E, F, O) were compared across backgrounds (quiet and noise) for all stimulus durations, across stimulus durations (50 and 170 msec) and across consonant–vowels ([ba], [da], and [ga]). Additionally, degree of phase locking to the stimulus fundamental frequency (in quiet versus noise) was evaluated for the frequency following response in speech-ABRs to the 170 msec [da]. Finally, the number of epochs required for a robust response was evaluated using F sp statistic and bootstrap analysis at different epoch iterations. Results: Background effect: the addition of background noise resulted in speech-ABRs with longer peak latencies and smaller peak amplitudes compared with speech-ABRs in quiet, irrespective of stimulus duration. However, there was no effect of background noise on the degree of phase locking of the frequency following response to the stimulus fundamental frequency in speech-ABRs to the 170 msec [da]. Duration effect: speech-ABR peak latencies and amplitudes did not differ in response to the 50 and 170 msec stimuli. Consonant–vowel effect: different consonant–vowels did not have an effect on speech-ABR peak latencies regardless of stimulus duration. Number of epochs: a larger number of epochs was required to record speech-ABRs in noise compared with in quiet, and a smaller number of epochs was required to record speech-ABRs to the 40 msec [da] compared with the 170 msec [da]. Conclusions: This is the first study that systematically investigated the clinical feasibility of speech-ABRs in terms of stimulus duration, background noise, and number of epochs. Speech-ABRs can be reliably recorded to the 40 msec [da] without compromising response quality even when presented in background noise. Because fewer epochs were needed for the 40 msec [da], this would be the optimal stimulus for clinical use. Finally, given that there was no effect of consonant–vowel on speech-ABR peak latencies, there is no evidence that speech-ABRs are suitable for assessing auditory discrimination of the stimuli used.

Endocochlear potential (EP) is essential for cochlear amplification by providing the voltage source needed to drive outer hair cell (OHC) transducer current, which leads to OHC electromechanical force. An early study using furosemide to reversibly reduce EP showed that distortion product otoacoustic emissions (DPOAEs) recovered before EP. This indicated that cochlear amplification may be able to adjust to a new, lower EP. To investigate the mechanism of this adjustment, the extracellular OHC voltage, which we term local cochlear microphonic (LCM), was measured simultaneously with DPOAE and EP while using intraperitoneal (IP) and intravenous injection of furosemide to reversibly reduce EP. With IP injection, the DPOAEs recovered fully, whereas the EP was reduced, but LCM showed a similar time course as EP. The DPOAEs failed to accurately report the variation of cochlear amplification. With intravenous injection, for which both reduction and recovery of EP are known to occur relatively quickly compared to IP, the cochlear amplification observed in LCM could attain nearly full or even full recovery with reduced EP. This showed the cochlea has an ability to adjust to diminished operating condition. Furthermore, the cochlear amplifier and EP recovered with different time courses: cochlear amplification just started to recover after the EP was nearly fully recovered and stabilized. Using a Boltzmann model and the second harmonic of the LCM to estimate the mechanoelectric transducer channel operating point, we found that the recovery of cochlear amplification occurred with recentering of the operating point.

Repeatedly pairing a brief train of vagus nerve stimulation (VNS) with an auditory stimulus drives reorganization of primary auditory cortex (A1), and the magnitude of this VNS-dependent plasticity is dependent on the stimulation parameters, including intensity and pulse rate. However, there is currently little data to guide the selection of VNS train durations, an easily adjusted parameter that could influence the effect of VNS-based therapies. Here, we tested the effect of varying the duration of the VNS train on the extent of VNS-dependent cortical plasticity. Rats were exposed to a 9 kHz tone 300 times per day for 20 days. Coincident with tone presentation, groups received trains of 4, 16, or 64 pulses of VNS delivered at 30 Hz, corresponding to train durations of 0.125 s, 0.5 s, and 2.0 s, respectively. High-density microelectrode mapping of A1 revealed that 0.5 s duration VNS trains significantly increased the number of neurons in A1 that responded to tones near the paired tone frequency. Trains lasting 0.125 or 2.0 s failed to alter A1 responses, indicating that both shorter and longer stimulation durations are less effective at enhancing plasticity. A second set of experiments evaluating the effect of delivering 4 or 64 pulses in a fixed 0.5 s VNS train duration paired with tone presentation reveal that both slower and faster stimulation rates are less effective at enhancing plasticity. We incorporated these results with previous findings describing the effect of stimulation parameters on VNS-dependent plasticity and activation of neuromodulatory networks to generate a model of synaptic activation by VNS.

Previous studies suggest that envelope-following responses (EFRs) reveal important differences in temporal coding fidelity amongst listeners who have normal hearing thresholds, consistent with these listeners differing in the degree to which they suffer from cochlear synaptopathy. Like conventional hearing loss, the severity of cochlear synaptopathy may vary along the cochlea. A number of earlier studies have suggested methods for estimating EFRs driven by specific frequency regions of the cochlea, which would allow synaptopathy to be estimated as a function of cochlear place. Here, we tested a method for measuring EFRs from multiple locations along the cochlea simultaneously, using narrowband stimuli. We compared responses to multiple simultaneous narrowband complex harmonic tones in three non-overlapping frequency bands, each having a unique fundamental frequency, to responses to the individual narrowband stimuli alone, and to responses when noise was added to different combinations of the frequency bands. Our results suggest that simultaneous presentation of multiple tone complexes with different fundamental frequencies leads to repeatable measures of temporal coding fidelity at the cochlear frequency regions corresponding to the narrowband carrier frequencies. Other results suggested that while off-frequency contributions to EFRs driven by narrowband signals (due to spread of excitation) can add destructively to the on frequency response, these interactions were small compared to EFR magnitude. Overall, our results point to the utility of using multi-band complex tone stimuli to estimate the profile of temporal coding fidelity, and thus the degree of synaptopathy, as a function of cochlear place. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.

The central gain model of hyperacusis proposes that loss of auditory input can result in maladaptive neuronal gain increases in the central auditory system, leading to the over-amplification of sound-evoked activity and excessive loudness perception. Despite the attractiveness of this model, and supporting evidence for it, a critical test of the central gain theory requires that changes in sound-evoked activity be explicitly linked to perceptual alterations of loudness. Here we combined an operant conditioning task that uses a subject's reaction time to auditory stimuli to produce reliable measures of loudness growth with chronic electrophysiological recordings from the auditory cortex and inferior colliculus of awake, behaviorally-phenotyped animals. In this manner, we could directly correlate daily assessments of loudness perception with neurophysiological measures of sound encoding within the same animal. We validated this novel psychophysical-electrophysiological paradigm with a salicylate-induced model of hearing loss and hyperacusis, as high doses of sodium salicylate reliably induce temporary hearing loss, neural hyperactivity, and auditory perceptual disruptions like tinnitus and hyperacusis. Salicylate induced parallel changes to loudness growth and evoked response-intensity functions consistent with temporary hearing loss and hyperacusis. Most importantly, we found that salicylate-mediated changes in loudness growth and sound-evoked activity were correlated within individual animals. These results provide strong support for the central gain model of hyperacusis and demonstrate the utility of using an experimental design that allows for within-subject comparison of behavioral and electrophysiological measures, thereby making inter-subject variability a strength rather than a limitation.

Purpose As pulse rate increases beyond a few hundred Hertz, younger normal-hearing (NH) participants' ability to encode temporal information in band-limited acoustic pulse trains decreases, demonstrating a rate limitation in processing rapid temporal information. Rate discrimination abilities, however, have yet to be investigated in older NH participants—a population that experiences age-related temporal processing deficits. It was hypothesized that age-related temporal processing deficits lead to decreased temporal rate discrimination abilities in older compared with younger NH participants, which could be observed in both perceptual and electrophysiological measurements. Method Fifteen younger and 15 older NH participants were presented acoustic pulse trains with a 4-kHz center frequency and 1-kHz bandwidth at 75 dB SPL monaurally. The pulse rate was 80, 200, or 400 Hz. Just noticeable differences were obtained using an adaptive procedure that instructed the participants to identify the pulse train with the highest pitch. Auditory steady-state responses (ASSRs) were recorded to the same pulse trains with 2 additional rates—20 and 40 Hz. The Digit Symbol Coding and Digit Symbol Search subtests of the Wechsler Adult Intelligence Scale ( Wechsler, 1997 ) were measured as correlates to domain-general cognitive processing speed. Results As rate increased from 80 to 400 Hz, performance on the perceptual rate discrimination task worsened in both groups. ASSR spectral energy also decreased, but only in the older group. Perceptual performance was equivalent between groups across rates. The older group had lower ASSR spectral energy (lower signal-to-noise ratios) at the 400-Hz rate than the younger group, but there were no group differences for the other rates. The overall strength of neural rate representation, along with speed of processing performance, predicted perceptual performance for the 400-Hz rate. Conclusion These results suggest that neural representation at early levels of the auditory system and processing speed are factors in perceptual auditory temporal processing performance, especially in older adults.

Technology that translates neural activity into speech would be transformative for people who are unable to communicate as a result of neurological impairments. Decoding speech from neural activity is challenging because speaking requires very precise and rapid multi-dimensional control of vocal tract articulators. Here we designed a neural decoder that explicitly leverages kinematic and sound representations encoded in human cortical activity to synthesize audible speech. Recurrent neural networks first decoded directly recorded cortical activity into representations of articulatory movement, and then transformed these representations into speech acoustics. In closed vocabulary tests, listeners could readily identify and transcribe speech synthesized from cortical activity. Intermediate articulatory dynamics enhanced performance even with limited data. Decoded articulatory representations were highly conserved across speakers, enabling a component of the decoder to be transferrable across participants. Furthermore, the decoder could synthesize speech when a participant silently mimed sentences. These findings advance the clinical viability of using speech neuroprosthetic technology to restore spoken communication.

Neuron–glia communication contributes to the fine-tuning of synaptic functions. Oligodendrocytes near synapses detect and respond to neuronal activity, but their role in synapse development and plasticity remains largely unexplored. We show that oligodendrocytes modulate neurotransmitter release at presynaptic terminals through secretion of brain-derived neurotrophic factor (BDNF). Oligodendrocyte-derived BDNF functions via presynaptic tropomyosin receptor kinase B (TrkB) to ensure fast, reliable neurotransmitter release and auditory transmission in the developing brain. In auditory brainstem slices from Bdnf+/– mice, reduction in endogenous BDNF significantly decreased vesicular glutamate release by reducing the readily releasable pool of glutamate vesicles, without altering presynaptic Ca2+ channel activation or release probability. Using conditional knockout mice, cell-specific ablation of BDNF in oligodendrocytes largely recapitulated this effect, which was recovered by BDNF or TrkB agonist application. This study highlights a novel function for oligodendrocytes in synaptic transmission and their potential role in the activity-dependent refinement of presynaptic properties.