About

Benjamin David Auerbach is an Assistant Professor in Molecular and Integrative Physiology, Neuroscience Program, and the Beckman Institute for Advanced Science and Technology at the University of Illinois. He is also an affiliate of the Carl R. Woese Institute for Genomic Biology. His research focuses on the neural mechanisms underlying sensory processing and plasticity, particularly how the brain modifies its connections and adapts its response properties based on prior experience. This experience-dependent plasticity is fundamental to learning and memory and is disrupted in various neurological and psychiatric disorders. Auerbach's work uses the rodent auditory system as a model to elucidate the biological mechanisms and behavioral consequences of experience-dependent brain modification. His multidisciplinary approach combines quantitative sensory behavior, high-density in vivo electrophysiology, ex vivo biochemical and neuroanatomical analysis, as well as optical imaging and manipulation of genetically-defined neuronal subtypes. Beyond advancing basic understanding of brain function, his research aims to identify pathophysiological mechanisms associated with neurodevelopmental and hearing disorders that often present with sound hypersensitivity, such as autism spectrum disorders and hyperacusis, with the goal of translating findings into novel therapies and treatment strategies.

Research topics

• Psychiatry
• Psychology
• Neuroscience
• Medicine
• Developmental psychology
• Internal medicine

Selected publications

• Cross-comparison of anesthetic regimens for auditory brainstem response recordings in rats

  Hearing Research · 2026-04-15

  articleOpen accessSenior authorCorresponding

  • Anesthetics for ABR recordings require trade-off between safety and signal quality • Xylazine with ketamine preserves signal but increases mortality and recovery time • Isoflurane weakened signal strength and reduced trial-to-trial reliability • Dexmedetomidine with ketamine preserves both safety and signal measures • Results guide more reliable anesthetic choices in pre-clinical hearing research Auditory brainstem response (ABR) recordings are widely used in neuroscience as a cross-species translational tool to evaluate hearing sensitivity and auditory processing. In animal models, ABR recordings typically require the use of anesthesia to minimize myogenic artifacts, necessitating the development of anesthetic regimens that balance safety, adequate immobilization, and preservation of neural responses. Using a within-subject design in male and female Long-Evans rats, this study systematically evaluated the safety and auditory signal fidelity of five anesthetic regimens—ketamine/xylazine (K/X), ketamine/dexmedetomidine (K/D), dexmedetomidine alone (DEX), dexmedetomidine plus low dose (0.5%) isoflurane (D/I), and high dose (2%) isoflurane (ISO). Anesthetic safety and efficacy were assessed by induction time, recovery time, blood oxygen saturation (SpO₂), and survival rate. ABR signal quality was quantified by threshold, signal strength, wave amplitude, wave latency, and inter-trial phase coherence. K/X anesthesia produced ABRs with low thresholds and well-defined waveforms, but also exhibited the least favorable safety profile, with prolonged recovery times and reduced survival rates. Conversely, isoflurane regimens (ISO and D/I) had a favorable safety profile but significantly elevated thresholds and degraded ABR signal quality, even at low doses. K/D and DEX achieved survival and recovery outcomes equal to or better than conventional anesthetics (K/X and ISO) while also preserving ABR waveform morphology and trial-to-trial reliability. Together, these results highlight dexmedetomidine, particularly when combined with ketamine, as a safe and effective anesthetic for ABR recordings that preserves key metrics of auditory sensitivity and signal integrity.

  PublisherDOI

• Altered auditory feature discrimination in a rat model of Fragile X Syndrome

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-19

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Atypical sensory processing, particularly in the auditory domain, is one of the most common and quality-of-life affecting symptoms seen in autism spectrum disorders (ASD). Fragile X Syndrome (FXS) is the leading inherited cause of ASD and a majority of FXS individuals present with auditory processing alterations. While auditory hypersensitivity is a common phenotype observed in FXS and Fmr1 KO rodent models, it is important to consider other auditory coding impairments that could contribute to sound processing difficulties and disrupted language comprehension in FXS. We have shown previously that a Fmr1 knockout (KO) rat model of FXS exhibits heightened sound sensitivity that coincided with abnormal perceptual integration of sound bandwidth, indicative of altered spectral processing. Frequency discrimination is a fundamental aspect of sound encoding that is important for a range of auditory processes, such as source segregation and speech comprehension, and disrupted frequency coding could thus contribute to a range of auditory issues in FXS and ASD. Here we explicitly characterized spectral processing deficits in male Fmr1 KO rats using an operant conditioning tone discrimination assay and in vivo electrophysiology recordings from the auditory cortex and inferior colliculus. We found that Fmr1 KO rats exhibited poorer frequency resolution, which corresponded with neuronal hyperactivity and broader frequency tuning in auditory cortical but not collicular neurons. Using an experimentally informed population model, we show that these cortical physiological differences can recapitulate the observed behavior discrimination deficits, with decoder performance being tightly linked to differences in cortical tuning width and signal-to-noise ratios. These findings suggest that cortical hyperexcitability may account for a range of auditory behavioral phenotypes in FXS, providing a potential locus for development of novel biomarkers and treatment strategies that could extend to other forms of ASD.

  PublisherOA PDFDOI

• Altered auditory feature discrimination in a rat model of Fragile X Syndrome

  PLoS Biology · 2025-07-01 · 1 citations

  articleOpen accessSenior author

  Atypical sensory processing, particularly in the auditory domain, is one of the most common and quality-of-life affecting symptoms seen in autism spectrum disorders (ASD). Fragile X Syndrome (FXS) is a leading inherited cause of ASD and a majority of FXS individuals present with auditory processing alterations. While auditory hypersensitivity is a common phenotype observed in FXS and Fmr1 knockout (KO) rodent models, it is important to consider other auditory coding impairments that could contribute to sound processing difficulties and disrupted language comprehension in FXS. We have shown previously that a Fmr1 KO rat model of FXS exhibits heightened sound sensitivity that coincided with abnormal perceptual integration of stimulus bandwidth, indicative of altered spectral processing. Frequency discrimination is a fundamental aspect of sound encoding that is important for a range of auditory processes, such as source segregation and speech comprehension, and disrupted frequency coding could thus contribute to a range of auditory issues in FXS and ASD. Here we explicitly characterized spectral processing deficits in male Fmr1 KO rats using an operant conditioning tone discrimination assay and in vivo electrophysiological recordings from the auditory cortex and inferior colliculus. We found that Fmr1 KO rats exhibited poorer frequency resolution, which corresponded with neuronal hyperactivity and broader frequency tuning in auditory cortical but not collicular neurons. Using an experimentally informed population model, we show that these cortical physiological differences can recapitulate the observed behavior discrimination deficits, with decoder performance being tightly linked to differences in cortical tuning width and signal-to-noise ratios. Together, these findings indicate that cortical hyperexcitability in Fmr1 KO rats may act to preserve signal-to-noise ratios and signal detection threshold at the expense of sound sensitivity and fine feature discrimination, highlighting a potential mechanistic locus for a range of auditory behavioral phenotypes in FXS.

  PublisherDOI

• Foxg1 gene mutation impairs auditory cortex response and reduces sound tolerance

  Cerebral Cortex · 2025-06-01 · 4 citations

  articleOpen access

  FOXG1 syndrome (FS) is a rare and devastating neurodevelopmental disorder affected by FOXG1 gene mutations and reduced sound tolerance has been reported in children with FS. Effects of single missense mutation of Foxg1 gene on auditory function and behavior were studied using the G216S mouse model. G216S mice showed significantly reduced gap-induced prepulse inhibition, suggesting poor temporal processing without hearing loss. Increased running and freezing behaviors under loud sounds were also found in G216 mice, suggesting aversive sound behaviors. Electrophysiological assessment of the auditory cortex of G216 mice revealed a slightly reduced amplitude and enlarged poststimulus responses to the sound stimulus. The layer function analysis using current source density revealed reduced layer-specific response in the G216S mice. Immunocytochemistry found Foxg1 gene mutation affects cortical layer differentiations and reduced cortical neurons, which are consistent with the physiological results. Our study suggests that the Foxg1 mutation impaired cortical development. The results are consistent with other models of autism spectrum disorders (ASDs), suggesting that the G216S mouse model may represent a hyperacusis model of ASD. Our results provide direct evidence that a single-nucleotide mutation of the Foxg1 gene can affect cortical layer development and auditory processing and reduce sound tolerance.

  PublisherOA PDFDOI

• REVIEW: HYPERACUSIS, ANIMAL MODELS, CHRONIC STRESS, AND AUTISM IN FRAGILE X

  Journal of Hearing Science · 2025-12-19

  articleOpen accessSenior author

  Hyperacusis is a loudness intolerance disorder associated with many medical conditions. To investigate the biological bases of hyperacusis in animals, we developed an auditory reaction time-intensity (RT-I) paradigm to assess the growth of loudness in rats treated with sodium salicylate, a drug suspected to cause hyperacusis. Loudness growth was unaffected by low-dose salicylate; however, high doses significantly reduced reaction times at high intensities, resulting in behavioral evidence of hyperacusis. To identify the neural correlates of salicylate-induced hyperacusis, neural activity was monitored along the auditory pathway. Salicylate significantly reduced the neural output of the cochlea. Paradoxically, neural responses were progressively amplified when relayed towards the central auditory pathway resulting in responses 2x larger than normal in auditory cortex (ACx), evidence of enhanced central gain. Because salicylate dose-dependently increased corticosterone stress hormone levels, rats were chronically fed corticosterone stress hormone to determine its behavioral and electrophysiological effects. This led to enhanced sound-evoked neural response in ACx without altering the neural responses from the cochlea and auditory brainstem. Patients with autism often suffer from sound tolerance issues (i.e., hyperacusis). Fragile X (FX) syndrome is a leading genetic cause of autism. To determine if rats with the FX mutation suffered from hyperacusis, we compared loudness growth functions in FX rats with littermate controls. FX rats had normal hearing thresholds but exhibited behavioral evidence of loudness hyperacusis and abnormal temporal and spectral integration of loudness. These behavioral models of hyperacusis can guide the search for biological bases of hyperacusis.

  PublisherOA PDFDOI

• Evaluating the feasibility of prehospital point‐of‐care EEG: The prehospital implementation of rapid EEG (PHIRE) study

  Journal of the American College of Emergency Physicians Open · 2024-09-13 · 13 citations

  articleOpen access

  Background: Point-of-care electroencephalography (EEG) devices can be rapidly applied and do not require specialized technologists, creating new opportunities to use EEG during prehospital care. We evaluated the feasibility of point-of-care EEG during ambulance transport for 911 calls. Methods: This mixed-methods study was conducted between May 28, 2022 and October 28, 2023. Emergency Medical Services (EMS) clinicians identified eligible individuals, provided emergent treatment, applied EEG, and obtained an EEG recording during ambulance transport. Eligible patients were aged 6 years or older and evaluated for seizure, stroke, or altered mental status. EMS clinicians completed a survey and a brief phone interview following every enrollment. Two epileptologists reviewed EEG recordings for interpretability and artifact. Results: There were 34 prehospital encounters in which EEG was applied. Patients had a mean age of 69 years, and 15 (44%) were female. EEG recordings had a median duration of 10 min 30 s. It took EMS clinicians an average of 2.5 min to apply the device and begin EEG recording. There were 14 (47%) recordings where clinicians achieved a high-quality connection for all 10 electrodes and 32 (94%) recordings that were sufficient in quality to interpret. There were 24 (71%) recordings with six or more channels free of artifact for 5 min or more. All clinicians agreed or strongly agreed that the device was easy to use. Conclusion: Among real-world prehospital encounters for patients with neurologic symptoms, point-of-care EEG was rapidly applied and yielded EEG recordings that could be used for clinical interpretation, demonstrating the feasibility of point-of-care EEG in future prehospital care.

  PublisherOA PDFDOI

• Editorial: Neural markers of sensory processing in development

  Frontiers in Integrative Neuroscience · 2023-07-21

  editorialOpen access

  EDITORIAL article Front. Integr. Neurosci., 21 July 2023 Volume 17 - 2023 | https://doi.org/10.3389/fnint.2023.1256437

  PublisherOA PDFDOI

• Hearing in Complex Environments: Auditory Gain Control, Attention, and Hearing Loss

  Frontiers in Neuroscience · 2022-02-10 · 36 citations

  reviewOpen access1st authorCorresponding

  Listening in noisy or complex sound environments is difficult for individuals with normal hearing and can be a debilitating impairment for those with hearing loss. Extracting meaningful information from a complex acoustic environment requires the ability to accurately encode specific sound features under highly variable listening conditions and segregate distinct sound streams from multiple overlapping sources. The auditory system employs a variety of mechanisms to achieve this auditory scene analysis. First, neurons across levels of the auditory system exhibit compensatory adaptations to their gain and dynamic range in response to prevailing sound stimulus statistics in the environment. These adaptations allow for robust representations of sound features that are to a large degree invariant to the level of background noise. Second, listeners can selectively attend to a desired sound target in an environment with multiple sound sources. This selective auditory attention is another form of sensory gain control, enhancing the representation of an attended sound source while suppressing responses to unattended sounds. This review will examine both "bottom-up" gain alterations in response to changes in environmental sound statistics as well as "top-down" mechanisms that allow for selective extraction of specific sound features in a complex auditory scene. Finally, we will discuss how hearing loss interacts with these gain control mechanisms, and the adaptive and/or maladaptive perceptual consequences of this plasticity.

  PublisherOA PDFDOI

• Auditory hypersensitivity and processing deficits in a rat model of fragile X syndrome

  Neurobiology of Disease · 2021-10-29 · 31 citations

  articleOpen access1st authorCorresponding

  Fragile X (FX) syndrome is one of the leading inherited causes of autism spectrum disorder (ASD). A majority of FX and ASD patients exhibit sensory hypersensitivity, including auditory hypersensitivity or hyperacusis, a condition in which everyday sounds are perceived as much louder than normal. Auditory processing deficits in FX and ASD also afford the opportunity to develop objective and quantifiable outcome measures that are likely to translate between humans and animal models due to the well-conserved nature of the auditory system and well-developed behavioral read-outs of sound perception. Therefore, in this study we characterized auditory hypersensitivity in a Fmr1 knockout (KO) transgenic rat model of FX using an operant conditioning task to assess sound detection thresholds and suprathreshold auditory reaction time-intensity (RT-I) functions, a reliable psychoacoustic measure of loudness growth, at a variety of stimulus frequencies, bandwidths, and durations. Male Fmr1 KO and littermate WT rats both learned the task at the same rate and exhibited normal hearing thresholds. However, Fmr1 KO rats had faster auditory RTs over a broad range of intensities and steeper RT-I slopes than WT controls, perceptual evidence of excessive loudness growth in Fmr1 KO rats. Furthermore, we found that Fmr1 KO animals exhibited abnormal perceptual integration of sound duration and bandwidth, with diminished temporal but enhanced spectral integration of sound intensity. Because temporal and spectral integration of sound stimuli were altered in opposite directions in Fmr1 KO rats, this suggests that abnormal RTs in these animals are evidence of aberrant auditory processing rather than generalized hyperactivity or altered motor responses. Together, these results are indicative of fundamental changes to low-level auditory processing in Fmr1 KO animals. Finally, we demonstrated that antagonism of metabotropic glutamate receptor 5 (mGlu5) selectively and dose-dependently restored normal loudness growth in Fmr1 KO rats, suggesting a pharmacologic approach for alleviating sensory hypersensitivity associated with FX. This study leverages the tractable nature of the auditory system and the unique behavioral advantages of rats to provide important insights into the nature of a centrally important yet understudied aspect of FX and ASD.

  PublisherDOI

• Auditory Hypersensitivity and Processing Deficits in a Rat Model of Fragile X Syndrome

  bioRxiv (Cold Spring Harbor Laboratory) · 2021-09-25 · 3 citations

  preprintOpen access1st authorCorresponding

  Abstract Fragile X (FX) syndrome is one of the leading inherited causes of autism spectrum disorder (ASD). A majority of FX and ASD patients exhibit sensory hypersensitivity, including auditory hypersensitivity or hyperacusis, a condition in which everyday sounds are perceived as much louder than normal. Auditory processing deficits in FX and ASD also afford the opportunity to develop objective and quantifiable outcome measures that are likely to translate between humans and animal models due to the well-conserved nature of the auditory system and well-developed behavioral read-outs of sound perception. Therefore, in this study we characterized auditory hypersensitivity in a Fmr1 knockout (KO) transgenic rat model of FX using an operant conditioning task to assess sound detection thresholds and suprathreshold auditory reaction time-intensity (RT-I) functions, a reliable psychoacoustic measure of loudness growth, at a variety of stimulus frequencies, bandwidths and durations. Male Fmr1 KO and littermate WT rats both learned the task at the same rate and exhibited normal hearing thresholds. However, Fmr1 KO rats had faster auditory RTs over a broad range of intensities and steeper RT-I slopes than WT controls, perceptual evidence of excessive loudness growth in Fmr1 KO rats. Furthermore, we found that Fmr1 KO animals exhibited abnormal perceptual integration of sound duration and bandwidth, with diminished temporal but enhanced spectral integration of sound intensity. Because temporal and spectral integration of sound stimuli were altered in opposite directions in Fmr1 KO rats, this suggests that abnormal RTs in these animals are evidence of aberrant auditory processing rather than generalized hyperactivity or altered motor responses. Together, these results are indicative of fundamental changes to low-level auditory processing in Fmr1 KO animals. Finally, we demonstrated that antagonism of metabotropic glutamate receptor 5 (mGlu5) selectively and dose-dependently restored normal loudness growth in Fmr1 KO rats, suggesting a pharmacologic approach for alleviating sensory hypersensitivity associated with FX. This study leverages the tractable nature of the auditory system and the unique behavioral advantages of rats to provide important insights into the nature of a centrally important yet understudied aspect of FX and ASD.

  PublisherOA PDFDOI

Recent grants

• The Role of Central Gain Control in Hyperacusis of Diverse Origin

  NIH · $183k · 2016–2019

• Mechanisms of sound hypersensitivity in a rat model of autism

  NIH · $715k · 2020–2026

Frequent coauthors

• Mark F. Bear

  Massachusetts Institute of Technology

  21 shared

• Richard Salvi

  University at Buffalo, State University of New York

  17 shared

• Emily K. Osterweil

  Boston Children's Hospital

  12 shared

• Kelly E. Radziwon

  Women & Children's Hospital of Buffalo

  10 shared

• Gül Dölen

  Discovery Institute

  8 shared

• Senthilvelan Manohar

  7 shared

• Xiaopeng Liu

  Women & Children's Hospital of Buffalo

  5 shared

• Robert J. Lefkowitz

  5 shared

Labs

• Auerbach Lab @ IllinoisPI

Awards & honors

• 2019 Travel Award for Association for Research in Otolaryngo…
• 2018-2019 NARSAD Young Investigator Award
• 2015, 2017 Bishops Award for Neuroscience, University at Buf…
• 2016 Blavatnik Award for Young Scientists Regional Nominee,…
• 2015 Society for Neuroscience Trainee Professional Developme…