# Mechanisms for cancelling self-generated sounds in the mouse dorsal cochlear nucleus

> **NIH NIH R01** · COLUMBIA UNIVERSITY HEALTH SCIENCES · 2020 · $340,000

## Abstract

Project Summary/Abstract
Our own movements result in patterns of sensory receptor activation that may be similar or identical to those
caused by external events. How does the brain make the critical distinction between self and other?
Longstanding theories suggest that proprioceptive feedback or internal copies of motor commands, known as
corollary discharge, could serve to predict and cancel out sensory input due to an animal’s own movements.
However, it has been difficult to understand where and how such a process actually takes place within the
brain. Some of the clearest insights come from cerebellum-like sensory structures associated with
electrosensory processing in fish. Work in these systems, including that of the PI, has shown that synaptic
plasticity acting on motor corollary discharge and proprioceptive information functions to predict and cancel out
self-generated electrosensory inputs related to the fish’s own behavior. This proposal seeks to understand
whether similar mechanisms are at work in the mammalian brain. Specifically, we focus on the dorsal cochlear
nucleus (DCN)--a structure at the initial stage of mammalian auditory processing which strikingly resembles
cerebellum-like structures in fish in terms of its circuitry and synaptic plasticity rules. We will use in vivo
recordings from awake, behaving mice to test whether non-auditory, movement-related input to DCN functions
to predict and cancel self-generated sounds associated with licking behavior. The proposed research is
expected to provide fundamental insight into the computations performed by the DCN, including an answer to
the longstanding question of why circuitry at the first stage of mammalian auditory processing resembles that
of the cerebellum. More generally, this work will provide mechanistic insights into how the mammalian brain
distinguishes between self-generated and external sources of sensory input. Finally, the common and in some
cases debilitating condition of tinnitus—the persistent perception of sound in the absence of an external sound
source—is associated with hyperactivity in DCN neurons and is hypothesized to be due, in part, to aberrant
synaptic plasticity and somatosensory integration in DCN. This project seeks to understand the normal function
of synaptic plasticity and somatosensory integration in DCN and hence may also provide insights into the
pathophysiology of tinnitus.

## Key facts

- **NIH application ID:** 9925765
- **Project number:** 5R01DC015449-05
- **Recipient organization:** COLUMBIA UNIVERSITY HEALTH SCIENCES
- **Principal Investigator:** Nathaniel Sawtell
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $340,000
- **Award type:** 5
- **Project period:** 2016-06-01 → 2021-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9925765

## Citation

> US National Institutes of Health, RePORTER application 9925765, Mechanisms for cancelling self-generated sounds in the mouse dorsal cochlear nucleus (5R01DC015449-05). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/9925765. Licensed CC0.

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