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Operational Mechanism of the ‘Acid-sensing Ion Channel’ that Recognizes Internal Body Pain

  • 조회. 533
  • 등록일. 2016.08.31
  • 작성자. Administrator

Operational Mechanism of the ‘Acid-sensing Ion Channel’ that Recognizes Internal Body Pain


team led by Professor Byung-Chang Suh identified the pain transmission

mechanism at the molecular level and presented new solutions for the

understanding of pain signals and the development of pain treatments.


Professor Byung-Chang Suh’s research team from the Department

of Brain and Cognitive Sciences succeeded in identifying a new operational

mechanism principle of the ‘Acid-sensing Ion Channel,’ which recognizes

internal pain in an organism.


The findings are expected to have a significant impact

on further studies focusing on the development of therapeutic agents that

control pain by providing a more precise understanding of the operational

mechanism of the ‘Acid-sensing Ion Channel’ that plays a pivotal role in

transmitting pain signals.


Pain is transmitted to the brain through nociceptive

nerves when pain spots that are distributed within an organism are stimulated.

Precisely, when pain causing substances are coupled to the plasma membrane of

the cells that constitute the pain spots, the pain signals are recognized.


Inside the organism, changes in pH levels occur under

pathophysiological conditions such as inflammation, ischemia, cancer, and the

like, which are accompanied by pain. The Acid-sensing Ion Channel (ASIC)

detects changes in pH levels in the organism and transmits the pain signal to

the brain. Biologically, many studies have been conducted regarding the Acid-sensing

Ion Channel; however, many areas are still unclear, especially in terms of the operational

mechanism and the cell membrane merging mechanism.   


Professor Suh’s research team detected the cell

membrane merging mechanisms that modulate the activity of the Acid-sensing Ion

Channel at the molecular level, and it is this discovery and identification of

the new cell membrane merging mechanism of the Acid-sensing Ion Channel that had

remained unknown until now.

The research team identified through animal

experiments that there is a different cell membrane merging mechanism between

subunits of the Acid-sensing Ion Channel. ASIC2a can be merged to cell membranes

and has a cell membrane merging signal in protein, unlike ASIC2b, which cannot

be merged to cell membranes. In addition, ASIC2b has no cell membrane merging

signal and can only be merged to the cell membrane by forming a heteromeric

complex with ASIC2a.


The outcome of this study is meaningful since it

identified a new cell membrane merging mechanism of the Acid-sensing Ion

Channel, and furthermore is significant that it proposed a research direction

for a new understanding of the activity control mechanism of various ion

channels among subunits including ASIC2, ASIC2b and many other subunits.


Professor Byung-Chang Suh from

DGIST’s Department of Brain and Cognitive Sciences said, “Understanding of the

cell membrane merging and activity control mechanism of the Acid-sensing Ion

Channel plays an important role in identifying the pain signal transmission

system. That our study investigated a new control mechanism of the Acid-sensing

Ion Channel has important implications. Through continuous research, I’ll

strive to identify additional operations that act on the nervous system and

will develop new ways to treat pain.”    


This research outcome was published in the online

edition of
Scientific Reports, a

sister publication to the international academic journal
Nature, on August 1, 2016. The study was conducted with the support

of junior executive researchers at the Ministry of Science, ICT, and Future

Planning; the Center for Nerve Aging and Regeneration Research at DGIST; and

the Center for Cerebral Cortex Research at the Korea Brain Research Institute.

Journal Reference

Hae-Jin Kweon, Byung-Chang Suh, et.

al., “Acid-Sensing Ion Channel 2a (ASIC2a) Promotes Surface Trafficking of

ASIC2b via Heteromeric Assembly”, Scientific Reports 2016.