Feinberg
Northwestern Medicine | Northwestern University | Faculty Profiles

News Center

  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Releases
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Menu
  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Releases
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Home » Protein Essential for Hearing Also Vital for Pain Perception
Uncategorized

Protein Essential for Hearing Also Vital for Pain Perception

By medwebJun 1, 2005
Share
Facebook Twitter Email

Protein Essential for Hearing Also Vital for Pain Perception

The same protein that “translates” sound into nerve signals to the brain and enables individuals to hear is also required for pain perception, researchers from Northwestern University’s Feinberg School of Medicine have found.

Because the protein, TRPA1, is found in most—about 75 percent—of the body’s pain-perceiving neurons, but not in major organs, drugs that could block TRPA1 would be novel painkillers with few or no side effects, although targeting the inner ear may have to be avoided, said Jaime Garcia-Añoveros, PhD, who led the research.

Dr. Garcia-Añoveros, assistant professor of anesthesiology, neurology, and physiology at the Feinberg School, a member of the Northwestern University Institute for Neuroscience (NUIN), and a fellow of the Hugh Knowles Center for Hearing Research, and colleagues described the dual role of TRPA1 in the cover article of the April 20 issue of the Journal of Neuroscience. His co-authors, all members of his research group at Northwestern University, were Keiichi Nagata, PhD, and Anne Duggan, PhD, both research assistant professors of anesthesiology, and Gagan Kumar, PhD, postdoctoral fellow in anesthesiology.

Dr. Garcia-Añoveros and his colleagues showed conclusive evidence that TRPA1, in addition to being expressed in nociceptors, or pain neurons, is present in the stereocilia of hair cells, the sensory part of the cells of the inner ear used for hearing as well as detecting gravity and maintaining balance.

Dr. Garcia-Añoveros and Dr. Duggan, also a NUIN researcher, initiated the study of TRPA1 in the late 1990s while searching for the channel that mediates hearing.

After they discovered that TRPA1 is expressed in the organ of Corti, the hearing organ of the inner ear, they were joined by colleagues at Harvard Medical School and Northwestern, and thus founded the groundbreaking group of scientists who in 2004 proposed that TRPA1 was a candidate for the mechanosensory channel of hair cells.

In the current study, the Northwestern researchers also demonstrated that TRPA1 channels have a unique combination of properties displayed by the hair cell transducer and by no other known channel. These similarities strongly suggest that TRPA1 is the pore that opens in response to sound, initiating the electrical signal cascade that ultimately reaches the brain as we perceive sounds.

The researchers have also found properties of the TRPA1 channel that account for its suspected parallel role in pain sensation, such as why in some cases pain from an injury will not go away as long as the injury remains.

Essentially, TRPA1 opens in response to painful stimulation, and ions enter the cell, making it less negatively charged, or depolarized. At this point most ion channels close, a phenomenon known as inactivation, because their signaling task has been achieved.

But TRPA1 senses the depolarization and responds to it by staying open; it will close only when the harmful stimulus goes away. However, if the depolarization is small, the TRPA1 channels close.

This means that TRPA1 could allow sensory neurons to ignore sustained innocuous stimuli (such as gentle pressure) but to respond to noxious stimuli (such as a pinch that causes tissue damage) and remain active as long as the noxious stimuli persist.

It also means that TRPA1 is sensitized by the opening of other nociceptor channels in the same sensory nerves; for example, those that respond to painful heat. This property of TRPA1 may thus account for painful phenomena in damaged tissues such as lack of desensitization or even some forms of enhanced sensitization, such as hyperalgesia (extreme sensitivity to pain) or allodynia (pain resulting from non-noxious stimuli to normal skin).

“Now we can look for TRPA1 channel blockers, which potentially will constitute novel analgesics that block pain at its initiation,” Dr. Garcia-Añoveros said.

“Such TRPA1 channel blockers should probably be used topically—preferably avoiding contact with the inner ear—but could also be applied systemically. In that case, the patient might have to put up with temporary deafness, a side effect that is probably better than extreme pain. What is critical at this point is to identify drugs or treatments that very specifically inhibit TRPA1,” he said.

TRPA1 is known to be activated by pain-producing chemicals such as the pungent components of edibles including wasabi, horseradish, mustard, cinnamon, and Listerine®, which explains why they sting the mouth.

This research was supported by grant RO1-NS044363 from the National Institute of Neurological Disorders and Stroke and grant R21-DC006089 from the National Institute on Deafness and Other Communication Disorders.

The full article is available online at http://www.jneurosci.org [25(16):4052-4061].

(Reprinted from the Northwestern University News Center.)

Share. Facebook Twitter Email

Related Posts

Lurie Cancer Center Receives Merit Extension from NCI

Oct 20, 2021

Drug Combination May Reduce Risk of Leukemia Relapse

Mar 26, 2020

Rewriting the Role of a Transcription Factor

Mar 19, 2020

Comments are closed.

Latest News

Hormone Therapy Plus Current Treatments Improves Survival in Prostate Cancer

Mar 22, 2023

How ChatGPT Has, and Will Continue to, Transform Scientific Research

Mar 21, 2023

New Directions for HIV Treatment

Mar 21, 2023

Humans are Not Just Big Mice: Identifying Science’s Muscle-Scaling Problem

Mar 20, 2023

AOA Honors New Members

Mar 20, 2023
  • News Center Home
  • Categories
  • Press Release
  • Media Coverage
  • Editor’s Picks
  • News Archives
  • About Us
Flickr Photos
20230315_NM036
20230315_NM046
20230315_NM134
20230315_NM205
20230315_NM206
20230315_NM132
20230315_NM130
20230315_NM082
20230315_NM063
20230315_NM058
20230315_NM030
20230315_NM038

Northwestern University logo

Northwestern University Feinberg School of Medicine

RSS Facebook Twitter LinkedIn Flickr YouTube Instagram
Copyright © 2023 Northwestern University
  • Contact Northwestern University
  • Disclaimer
  • Campus Emergency Information
  • Policy Statements

Type above and press Enter to search. Press Esc to cancel.