# Neural mechanisms of sound intensity coding

> **NIH NIH R01** · UNIV OF MARYLAND, COLLEGE PARK · 2020 · $323,000

## Abstract

Project Summary.
 A detailed understanding of the neurophysiological basis of hearing is fundamental to the
understanding of human hearing impairment and the guidance of further development of the most
successful prosthetic intervention to date, the cochlear implant. Yet we still lack a complete description of
how sound information is processed at even the first central nervous system relay, the cochlear nucleus.
Our experiments in the avian model system focus on the first central nervous system target of the
auditory nerve, the cochlear nucleus angularis, which initiates the ascending pathways involved in
localization using binaural sound level cues and spectrotemporal processing.
 Rapid adaptation is crucial for neural coding of complex sounds and scenes by implementing
temporal filtering, dynamic range adaptation and generating noise-invariant signal representations.
Dynamic range adaptation occurs when auditory neurons adjust their firing rate-level encoding
depending on the statistics of the acoustic stimulation, shifting upward with louder sound distributions.
Adaptive cellular processes such as short-term synaptic plasticity (activity-dependent alterations in
synaptic weight), intrinsic firing rate adaptation (via ion channel inactivation or hyperpolarizing currents),
and modulatory transmitter feedback via second messenger systems are all candidate mechanism for
implementing intensity-related adaptation. Using a combination of in vitro physiology, modeling and in
vivo recordings, we will investigate an intrinsic mechanism called threshold adaptation and its reliance on
the inactivation of sodium channels. We also test the hypothesis that short-term synaptic plasticity
contributes to solving the `dynamic range problem': how human can hear across many orders of intensity
magnitude in behavioral experiments given the (formerly known) limited physiological range of nerve
fibers.
 Given the recent advances in the restoration of hearing using prosthetic devices that stimulate the
auditory nerve, it is critical to understand how nerve activity is interpreted by the central nervous system.
This research will provide new data on how acoustic information is transmitted from the auditory nerve to
the first central relay in normal hearing, and thus can provide a reference for devices such as cochlear
implants that stimulate the nerve directly. The emphasis on temporal envelope coding may also provide
new information on disorders that may be related to disrupted temporal processing, such as age-related
hearing loss or auditory neuropathy, which can lead to a common but disabling difficulty with
understanding speech in noise.

## Key facts

- **NIH application ID:** 9952340
- **Project number:** 5R01DC010000-10
- **Recipient organization:** UNIV OF MARYLAND, COLLEGE PARK
- **Principal Investigator:** KATRINA M MACLEOD
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $323,000
- **Award type:** 5
- **Project period:** 2010-03-01 → 2022-09-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9952340

## Citation

> US National Institutes of Health, RePORTER application 9952340, Neural mechanisms of sound intensity coding (5R01DC010000-10). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9952340. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*