# Role of Adaptive Myelination in Auditory Brain Plasticity

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2021 · $506,636

## Abstract

Project Summary/ Abstract:
Early auditory experience is crucial for establishing and remodeling neural circuits in the auditory brain. A loss
of peripheral sound input in congenital and early-onset deafness structurally and functionally alters central
auditory circuits, even after peripheral sound sensitivity is restored with hearing aids. To prevent and reverse
central auditory dysfunctions following peripheral hearing deficits, it is important to understand how plasticity in
the auditory brain creates new connections between restored sound input and central auditory processing
centers. Our previous studies showed that myelin was an important feature in resolving auditory signals with
extreme temporal precision for central auditory processing. Sound input itself is critical for myelin development
and maintenance along auditory brainstem circuitry throughout life. However, the extent to which auditory
experience-regulated myelin development and plasticity contribute to central auditory processing, and how
adaptive myelination occurs in the auditory brainstem, are unclear. The goal of this proposal is to determine the
cellular mechanisms whereby auditory experiences regulate auditory brain plasticity and central processing via
adaptive myelination. Our recent studies pioneered a new concept in understanding communication between
neurons and myelin-forming cells, oligodendrocytes (OLs) by defining OL excitability in the auditory brainstem.
A new subpopulation of OLs expresses glutamate receptors, voltage-gated Na+ (Nav), and Ca2+ channels, which
underlie OL depolarization, Na+ current-mediated spiking and Ca2+ dynamics. Thus, these OLs are ideally poised
to communicate with electrically active neurons and reward with increased myelination. Based on these data,
we hypothesize that increased sound-evoked activity enhances electrical and chemical communication
between this novel class of excitable OLs and neurons to regulate OL development and drives adaptive
myelination for fine-tuning temporal fidelity of auditory impulses. To test this hypothesis, we will utilize sound
modification (stimulation or deprivation), in vivo and ex vivo electrophysiology (auditory brainstem responses
and patch-clamp recordings), intracellular Ca2+ imaging, and anatomical analysis techniques. We will determine
how sound stimulation modulates neuron-OL communication and OL excitability (Aim 1), how OL excitability
enhances adaptive myelination (Aim 2), and how loss of Nav1.2-mediated OL excitability impacts adaptive
myelination and auditory brainstem circuitry (Aim 3). The proposed study will provide novel mechanistic insights
into how peripheral auditory signals contribute to adaptive myelination and neural plasticity via neuron-
oligodendroglia communication in the auditory brain. Elucidating the mechanisms of sound-driven adaptive
myelination is essential for understanding auditory brain plasticity during development and for developing an
effective therapeutic strategy ...

## Key facts

- **NIH application ID:** 10210896
- **Project number:** 1R01DC018797-01A1
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **Principal Investigator:** Jun Hee Kim
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $506,636
- **Award type:** 1
- **Project period:** 2021-04-01 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10210896

## Citation

> US National Institutes of Health, RePORTER application 10210896, Role of Adaptive Myelination in Auditory Brain Plasticity (1R01DC018797-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10210896. Licensed CC0.

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