Patrick D. Parker, Ph.D.
Meet the Researcher
Parker received his doctorate in neuroscience at the University of Utah, where he studied astrocyte management of glutamate signaling in a model of familial hemiplegic migraine. He is currently a postdoctoral fellow in the lab of Dwight Bergles, Ph.D., in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins School of Medicine. Parker studies the brain effects of hearing loss, with a particular interest in spontaneous activity and changes in inhibition during sound processing. His expertise is in combining genetic and optical methods to explore brain physiology in living animal models. Parker’s 2026 Emerging Research Grant is generously funded by the Les Paul Foundation.
Secondary disorders develop alongside hearing loss, such as the perception of phantom sounds (tinnitus) and a hypersensitivity to sound (hyperacusis). These disorders have no curative treatment, in part due to our poor understanding of the underlying neurobiology. Using experimental models of hearing loss, I recently discovered that sound-independent (SI) patterns of neural activity emerge in the brain’s auditory centers that resemble those elicited by sound in hearing mice. This finding indicates that the brain can self-generate neural patterns that resemble sound processing, independent of the inner ear. To understand the relevance of SI activity to human disorders like tinnitus, I’ll expand these findings to more translationally relevant models of hearing loss (loud noise exposure and age-related hearing loss), as well as determine the area of the brain that generates these patterns. The results of these studies may help to develop new approaches to treat tinnitus, hyperacusis, and related disorders.
Approximately 29 percent of U.S. adults in their 50s report some level of hearing loss, and this number grows to 69 percent of individuals in their 70s. Beyond social isolation and a decrease in quality of life, hearing loss has a much broader societal impact, as it has been linked to dementia, cognitive decline, and a decrease in total brain volume in older adults, as well as disorders of sound perception, like tinnitus and hyperacusis. However, the diverse sequelae that follow the loss of sensory input are not well defined, and the cellular changes in the brain that link hearing loss to secondary disorders are uncertain. The long-term goals related to this project are to determine the locus (or loci) of tonotopically patterned sound-independent activity in the CNS to guide mechanistic studies into how these patterns arise. Thus, these studies will provide new insight into the basic biology of hearing-related disorders, which could spawn new therapeutic avenues.
The discovery that spontaneous activity is tonotopically coordinated after hearing loss arose by chance from a collaboration with Ulrich Mueller, Ph.D., and Riley Bottom, Ph.D., who study the basic biology of mechanoelectrical transduction in hair cells. They had developed several new mouse models with varying degrees of hearing loss, and we wanted to test the influence of different levels of hearing loss on sound processing in the central nervous system.
I was particularly interested in studying a mouse with complete hearing loss. This confused everyone, because what can you learn about changes in sound processing from an animal that can’t hear sound? Truthfully, I didn’t have an answer, but I knew that the auditory areas of the brain would be doing something. Those neurons that used to process sound would still be active and would still be synaptically connected to one another and to the rest of the brain. What would activity in that network—a collection of 10s to 1,000s of neurons or more—look like? I didn’t know what to expect, but I was curious. And if there wasn’t anything interesting to see, it would be a short experiment.
Most of the previous work on hearing loss focused on individual neurons or small networks of neurons. I chose to record from the surface of the entire midbrain in an awake mouse using an optical recording method available in Dr. Dwight Bergles’ lab, where I’m a postdoctoral fellow. From the first recording, I knew we had found something remarkable: patterns of spatially coordinated neural activity in a deafened mouse that resembled sound processing in a hearing animal. Tonotopy without sound.
The recordings of brain neural activity looked as if the mouse was listening to a recording of random tones, or as if someone was haphazardly pressing keys on a piano. The groups of neurons that used to respond to a particular sound frequency were still coordinating their firing with one another after the loss of mechanoelectrical transduction in hair cells. Somehow, spontaneous, sensory-like brain patterns had emerged after sensory loss.
This chance discovery is now the basis for the current Emerging Research Grant. I plan to leverage this mouse model to understand how internally generated tonotopic patterns arise in the brain after hearing loss and what that might reveal about the neurobiology of hearing-related disorders like tinnitus and hyperacusis.
I came to science through psychology/psychiatry, first as a technician at a residential facility, then as a case manager for individuals on psychiatric disability. I have always been interested in disorders of perception and distortions of reality. I learned during that time, though, just how few treatment options were available and, for many, how ineffective they can be. I attributed this shortcoming to our limited understanding of how the brain functions normally, let alone in disease. How can we expect to fix something if we don’t know how it works in the first place? So, I changed my career path to study basic neuroscience and decided that neurological disorders were more tractable and had better potential for improving treatments.
My father-in-law developed sudden sensorineural hearing loss about 1.5 years ago, after I had already begun working in animal models of induced hearing loss. It has been fascinating to draw parallels between his personal experience and what I see in the lab. His frustration with invasive tinnitus and difficulty hearing over any ambient noise has been an invaluable window into just how disruptive these conditions are. Thankfully, he has regained most of his hearing, and his invasive tinnitus has subsided, though he has a persistent high-pitched ringing.
Three career highlights are 1) when I discovered glutamatergic “plumes” during graduate school; 2) discovering that spontaneous activity is tonotopically organized after hearing loss during my postdoc; and 3) dissecting a human brain for a photoshoot with National Geographic while at the Allen Institute for Brain Science.
It is hard to imagine not being in research, but I would have also enjoyed neurology or running a company centered around therapeutics. I did step away from science for a few years to play music with a band in Seattle. The band mostly played a blend of psychrock and heavy metal, with extended jams. I was the singer and auxiliary person—guitar, bass, trumpet, keyboard, percussion, vocoder—filling in on whatever was needed. I also played singer-songwriter acoustic music. I had a lot of fun and it was a great period of my life!
I love the outdoors and exploring the mountains. I’m an avid rock climber and met my wife through the climbing community in Seattle. I also love fishing, kayaking, backcountry skiing, cycling, and exploring the woods. Being outdoors is re-energizing and helps me focus my thoughts around my research. During graduate school at the University of Utah, I would “lab binge”—working continuously for several days—then disappear to the Utah desert for an adventure. By the time I returned to the lab in Salt Lake City, I usually had new ideas for experiments or a new interpretation of recent results.
I plan to build my own independent research group centered around gain disorders of the central nervous system. Our main focus will be on hearing loss and related disorders (e.g., tinnitus, hyperacusis, and central processing disorder). Over time, we will extend into other gain disorders that involve disruptions in sensory processing, including sound, such as migraine and chronic pain (my Ph.D. thesis was in migraine). I also want to explore the potential of gene therapies and collaborate with companies to strategize the translational potential of our basic science work.
The Research
Patrick D. Parker, Ph.D. | Johns Hopkins University School of Medicine
Emergence of tonotopically organized spontaneous activity in the brain after genetic disruption of MET channel
Secondary disorders develop alongside hearing loss, such as the perception of phantom sounds (tinnitus) and a hypersensitivity to sound (hyperacusis). These disorders have no curative treatment, in part due to our poor understanding of the underlying neurobiology. Using experimental models of hearing loss, I recently discovered that sound-independent (SI) patterns of neural activity emerge in the brain’s auditory centers that resemble those elicited by sound in hearing mice. This finding indicates that the brain can self- generate neural patterns that resemble sound processing, independent of the inner ear. To understand the relevance of SI activity to human disorders like tinnitus, I’ll expand these findings to more translationally relevant models of hearing loss (loud noise exposure and age-related hearing loss), as well as determine the area of the brain that generates these patterns. The results of these studies may help to develop new approaches to treat tinnitus, hyperacusis, and related disorders.
Long-term goal: Approximately 29 percent of U.S. adults in their 50s report some level of hearing loss, and this number grows to 69 percent of individuals in their 70s. Beyond social isolation and a decrease in quality of life, hearing loss has a much broader societal impact, as it has been linked to dementia, cognitive decline, and a decrease in total brain volume in older adults, as well as disorders of sound perception, like tinnitus and hyperacusis. However, the diverse sequelae that follow the loss of sensory input are not well defined, and the cellular changes in the brain that link hearing loss to secondary disorders are uncertain. The long-term goals related to this project are to determine the locus (or loci) of tonotopically patterned sound-independent activity in the CNS to guide mechanistic studies into how these patterns arise. Thus, these studies will provide new insight into the basic biology of hearing-related disorders, which could spawn new therapeutic avenues.
Generously funded by the Les Paul Foundation
