Research OverviewAt the NEAF Lab, we investigate learning-induced neuroplasticity that promotes sound-cued behaviors in the auditory system, spanning from cellular to systems levels. We also investigate how abnormal neuroplasticity- both molecular and neural- lead to deficits in sound processing, as seen in language and communication disorders, such as autism.
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Current work in the lab tackles the following questions:
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to How does astrocyte diversity shape auditory circuits and function?
The auditory cortex is composed of a rich diversity of cell types, each with its own transcriptional identity. We recently discovered remarkable heterogeneity across these cell types, including distinct transcriptomic profiles within astrocyte populations. Yet, how these molecular signatures translate into functional roles within neural circuits remains largely unknown. To bridge this gap, our laboratory investigates the functional contributions of astrocytes using gene-targeted approaches, including adeno-associated viral (AAV) strategies. Our goal is to uncover how astrocytes- especially different subclusters- interact with neurons, shape auditory circuit activity, and influence sound-cue behavior. By understanding how their heterogenity contributes to astrocyte-mediated modulation of neural circuits and behavior, we aim to reveal fundamental principles of astrocyte–neuron interactions in the auditory brain. Moreover, we seek to apply this knowledge to abnormal temporal processing which is a major cause of prevalent language and communication disorders, with the goal of enhancing auditory function for improved sound comprehension and communication abilities. We are collaborating with the Muñoz-Ballester lab at University of Maryland, Baltimore County (UMBCC) to determine the structural organization of the astrocytes in the auditory cortex. |
Could the auditory system provide prodromal biomarkers of neurodevelopmental derailment?
Sound processing, auditory learning and memory are deeply interconnected. Auditory learning enhances sound processing, which underlies adaptive auditory behaviors. Failure of learning induced neuroplasticity that facilitate adaptive sound processing in the brain- and, consequently adaptive listening in the acoustic environment during development- may contribute to the sound discrimination impairments observed in autism. Prior research in neurotypical animals has shown subcortical correlates of successful temporal cue discrimination learning, which can be enhanced by inhibiting of histone deacetylase 3 (HDAC3), an epigenetic modulator. This finding suggests that the subcortical auditory system plays a crucial role in supporting adaptive changes to sensory-cognitive behaviors. Building on this, we leverage auditory signals as a window into early changes in auditory processing that may contribute to impairments in communication skills and listening abilities. Using innovative rat models of autism, we aim to determine whether neurophysiological and behavioral read-outs of auditory function can predict neurodevelopmental derailment? Our current work focuses on developing prodromal biomarkers of neurodevelopmental disorders. In collaboration with the Torres (SMIL) Lab at Rutgers we are investigating the potential use of Auditory Brainstem Responses (ABRs)- a neurophysiological signal that can be evoked in response to complex speech sounds and is readily accessible in humans- as a non-invasive, accessible and sensitive biomarker to screen, monitor and track the treatment effectiveness of neurodevelopmental disorders. We are extending this work to human neonates with collabaration with Dr. Marta Rogido at MidAtlantic Neonatology Associates (MANA) to determine the early neural markers of neurodevelopmental disorders in NICU babies. |
Can chromatin remodeling rescue auditory processing deficits in autism spectrum disorders models?
Individuals with autism spectrum disorders (ASD) often exhibit altered sensory processing and deficits in language development. Similary, rat models of autism show deficits in auditory cortical processing and exhibit abnormal neural activity to sounds. Previous research has shown that inhibiting HDAC3 in a sound-reward task that required temporal cue (AM rate) discrimination led to highly specific enhancements in AM rate processing. Learning-induced neural enhancements in temporal processing also correlated with long-term improvements in behavioral discrimination of temporal cues in wild-type adult rats. Current work will expand on this knowledge to rescue cortical processing deficits in genetic rat models of austim by manipulating plasticity in the auditory system. Specifically, we investigate how abnormal neuroplasticity underlying auditory temporal processing contributes to the pathogenesis of language and communication disorders. We aim to determine whether epigenetic remodeling can ameliorate known deficits by chnaging the gene expression patterns in different cell types across the lifespan in genetic rat models of austim. |
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Biomedical Research Institute of New Jersey 140 E. Hanover Ave., Cedar Knolls, NJ 07927 Phone: 973- 294 1757 |
