Jennifer Resnik, Ph.D.

Meet the Researcher

Resnik received a doctorate in neuroscience from the Weizmann Institute of Science in Israel and is currently a postdoctoral research fellow at Mass Eye and Ear, Harvard Medical School. Resnik’s 2017 Emerging Research Grant is funded by Hyperacusis Research Ltd.

Sensorineural hearing loss due to noise exposure, aging, or certain drugs or diseases reduces the neural activity transmitted from the cochlea to the central auditory system. These types of hearing loss often give rise to hyperacusis, an auditory hypersensitivity disorder in which low-to-moderate-intensity sounds are perceived as intolerably loud or even painful.

Previously thought as originating in the damaged ear, hyperacusis is emerging as a complex disorder. While it can be triggered by a peripheral (external) injury, it develops from a maladaptation of the central auditory system to the peripheral dysfunction. In other words, the brain, in trying to fix one thing, damages another.

The recovery of sound detection and speech comprehension accompanied by an increase in sound sensitivity may reflect an “overcompensation”—that drives the recovery of basic signal representations but also pushes central networks toward unstable states of heightened excitability and gain.

We want to better understand the paradoxical role of central auditory system plasticity as both the cause of—and treatment for—the perceptual consequences of hearing loss. To do this we are studying the brain’s compensatory mechanisms, after cochlear damage, that allow for basic sound recovery but also introduce chronic hypersensitivity, such as hyperacusis. Then we need to figure out how to use these mechanisms to our advantage, in order to improve how the brain processes sound after hearing loss.

As a child curious about how things work, I remember wondering, Can animals understand speech How do they communicate with one another? Now I wonder, how does the brain modify its own circuits and functions in order to navigate through dynamic environments and evolving sensory needs? By this I mean changes in the environment, like the lack of light or a lot of noise, or changes in the signal, such as talking to someone who has an accent. All of these affect how our brain interprets sound.

My audiogram shows typical hearing, but I know I have problems understanding speech in noisy environments, unless the person is standing right next to me. There isn’t yet a test (for humans) to diagnose “hidden hearing loss”—difficulty hearing speech in noise—but I sometimes wonder if it could be that.

Spanish is my mother tongue, since I grew up in Argentina. Then I lived and studied in Israel and learned Hebrew, and now I am the U.S. using English. So I speak three different languages, which makes me think about speech sounds, meanings, accents, and tones on a daily basis.

Jennifer Resnik, Ph.D.’s grant is funded by Hyperacusis Research Ltd. for her work investigating hyperacusis. We thank Hyperacusis Research for its support of studies examining hyperacusis and other severe forms of loudness intolerance.

The Research

Mass Eye and Ear, Harvard Medical School
Homeostatic modifications in cortical GABA circuits enable states of hyperexcitability and reduced sound level tolerance after auditory nerve degeneration

Sensorineural hearing loss due to noise exposure, aging, ototoxic drugs, or certain diseases reduce the neural activity transmitted from the cochlea to the central auditory system. These types of hearing loss often give rise to hyperacusis, an auditory hypersensitivity disorder in which low- to moderate-intensity sounds are perceived as intolerably loud or even painful. Previously thought as originating in the damaged ear, hyperacusis is emerging as a complex disorder. While it can be triggered by a peripheral injury, it develops from a maladaptation of the central auditory system to the peripheral dysfunction. My research will test the hypothesis that the recovery of sound detection and speech comprehension, may cause an overcompensation that leads to an increase in sound sensitivity and reduced tolerance of moderately loud sounds. 

This hypothesis will be tested using a combination of chronic single-unit recordings, operant behavioral methods and optogenetic interrogation of specific sub-classes of cortical interneurons. By understanding how brain plasticity is modulated, we will gain deeper insight into the neuronal mechanism underlying aberrant sound processing and its potential reversal.

Long-Term Goal: To better understand the paradoxical role of central auditory system plasticity as both the cause of—and treatment for—the perceptual consequences of hearing loss. A major step to reach this goal is to understand the compensatory mechanisms, following cochlear damage, that allow for basic sound recovery while potentially introducing hypersensitivity and causing chronic sensory impairments such as hyperacusis.