# Molecular epigenetic mechanisms that transform the auditory system for learning and memory

> **NIH NIH R01** · RUTGERS, THE STATE UNIV OF N.J. · 2022 · $83,163

## Abstract

PROJECT SUMMARY & ABSTRACT
 This goal of this project is to investigate epigenetic neural mechanisms that can ensure meaningful sounds
are faithfully and adaptively represented in the adult auditory brain. One important aspect of this research
concerns the precision of acoustic content in memory, which is important for learning and performing fine-tine
auditory discriminations. A second, concerns long-term maintenance of experience via learning-induced
neuroplasticity for strong auditory memory, which is relevant to maintain learned auditory abilities for life.
 Animals (including humans) use associative learning to link sound cues to salient events (like rewards or
other significant outcomes). When neural mechanisms of memory formation are activated following these
experiences—mechanisms that span from molecules to genes to circuits and systems—associative memory is
formed, which in turn provides otherwise arbitrary sound with acquired significance. For example, in audition,
communication abilities require that sounds are precisely linked with their learned meaning, which depends on
neuroplasticity and enduring auditory memory that lasts from minutes, to hours and days, or a lifetime. Decades
of research indicate that associative learning systematically changes the sensory cortex to alter representation
of sensory cues with learned behavioral salience. But why do some individuals naturally form auditory memories
stronger and more specifically than others? Epigenetic mechanisms that control chromatin acetylation by histone
deacetylases (HDACs) likely function to control genes that ultimately establish changes to the auditory system
that contribute to its plasticity and subsequent long-term auditory memory. Indeed, HDACs are capable of
controlling how much auditory cortex changes with meaningful experiences, which may provide an instructive
control on the auditory system as a whole for adaptive (or sometimes maladaptive) function. Currently unknown
are the downstream gene and circuit mechanisms with which HDACs regulate auditory cortical plasticity.
 This proposal is for an administrative supplement that would promote diversity in the research team
and in the field at large, here in particular to support a predoctoral trainee, Ms. Guan-En Graham, in her
final PhD years. Her research is within the scope and critical to the completion of behavioral pharmacological
and molecular work (parent AIM1) as well as viral (AIM2) techniques to manipulate HDAC3 in a rodent behavioral
model of auditory associative learning to determine how HDACs alter the acquisition and initial storage of robust
auditory memory. The studies will explain how HDACs regulate neuroplasticity from genes, molecules, circuits
and systems for robust auditory behaviors with a system better “tuned-in” to important sounds. This research
promotes neuroepigenetics and gene-discovery as an important new niche for auditory neuroscience. Trainee
support will set the stage for Guan-En’s resear...

## Key facts

- **NIH application ID:** 10666170
- **Project number:** 3R01DC018561-03S1
- **Recipient organization:** RUTGERS, THE STATE UNIV OF N.J.
- **Principal Investigator:** Kasia Bieszczad
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $83,163
- **Award type:** 3
- **Project period:** 2020-09-15 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10666170

## Citation

> US National Institutes of Health, RePORTER application 10666170, Molecular epigenetic mechanisms that transform the auditory system for learning and memory (3R01DC018561-03S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10666170. Licensed CC0.

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